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102 publications mentioning hsa-mir-215 (showing top 100)

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-215. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 247
Other miRNAs from this paper: hsa-mir-132, hsa-mir-144, hsa-mir-200c
The associations between miR-215 expression and various clinicopathological parameters of NSCLC tissues are presented in Table I. The patients were divided into a high miR-215 expression group and a low miR-215 expression group, using the median miR-215 expression value amongst all 115 NSCLC patients as a cut-off. [score:9]
To selectively overexpress or downregulate miR-215, mature miR-215 mimics or miR-215 inhibitors were transfected into A549 or 95D cells. [score:8]
Since among the 4 NSCLC cell lines the A549 cell line exhibited the lowest miR-215 expression, while 95D cells expressed relatively high levels of miR-215, these two cell lines were selected for miR-215 mimics or miR-215 inhibitor transfection and further analysis. [score:7]
In order to identify potential mRNA targets of miR-215, database searches of microRNA target prediction engine TargetScan (http:www. [score:7]
Using the bioinformatics software TargetScan for target gene prediction, ZEB2 was identified as a potential target of miR-215. [score:7]
Overexpression of miR-215 significantly inhibited cell proliferation, invasion and migration, promoted cell apoptosis in vitro and suppressed tumorigenicity in vivo. [score:7]
RT-qPCR analysis of the tumor tissues confirmed elevated miR-215 expression levels in miR-215 -overexpressing tumors (Fig. 4D) RT-qPCR analysis was performed to detect miR-215 expression in NSCLC tissues and cell lines. [score:7]
RT-qPCR analysis confirmed enhanced miR-215 expression following miR-215 mimics transfection and reduced miR-215 expression following miR-215 inhibitors transfection (Fig. 2A). [score:7]
RT-qPCR analysis of the tumor tissues confirmed elevated miR-215 expression levels in miR-215 -overexpressing tumors (Fig. 4D) The dysregulation of miRs has been demonstrated to be involved in tumorigenesis and progression in various types of tumor; however, their potential roles in NSCLC have remained to be elucidated. [score:6]
As demonstrated in Fig. 2D, upregulation of miR-215 inhibited the invasion of A549 cells. [score:6]
miR-215 expression is downregulated in NSCLC. [score:6]
To further confirm that ZEB2 is the direct target of miR-215 in NSCLC, miR-215 mimics were transfected into A549 cells, which significantly reduced ZEB2 protein expression levels in these cells (Fig. 3B). [score:6]
The pGL3-ZEB2-mut vector was constructed using ZEB2 that had undergone site-directed mutagenesis of the miR-215 target site using the Quik-Change site-directed mutagenesis kit (Agilent Technologies GmbH, Waldbronn, Germany). [score:5]
Notably, a number of miRs, including miR-132 (24), miR-144 (25) and miR-200c (26), participate in the regulation of ZEB2 activity in various tissues; however, the potential regulatory effect of miR-215 on ZEB2 expression in NSCLC has not been confirmed. [score:5]
Increased miR-215 expression suppresses xenograft tumor formation. [score:5]
Reduced miR-215 expression levels in colorectal cancer were found to be associated with increased tumor sizes and decreased disease-free survival times following radical surgery (27, 28). [score:5]
With regard to miR-215, several targets have been determined in previous studies, including protein tyrosine phosphatase receptor type T (11), thymidylate synthase (TS) (29), dihydrofolate reductase (29), retinoblastoma tumor suppressor gene 1 (RB1) (12), activated leukocyte cell adhesion molecule (ALCAM) (31) and activin receptor type 2B (32). [score:5]
Ectopic expression of miR-215 inhibited cell proliferation and triggered cell cycle arrest at G2 phase in HCT 116 colon cancer cells (29), and reduced cellular migration and invasion in an RCC cell line mo del (16). [score:5]
By contrast, miR-215 expression has been observed to be significantly reduced in esophageal adenocarcinoma (14), colon cancer (15) and renal cell carcinoma (RCC) (16), and in these cases it functions as a candidate tumor suppressor. [score:5]
The miR-215 expression in the 4 NSCLC cell lines was also markedly downregulated, compared with that of the NLECs (Fig. 1B). [score:5]
In addition, ZEB2 was identified as a direct target of miR-215. [score:4]
White et al (16) demonstrated that miR-215 directly targets ZEB2 in RCC. [score:4]
For example, miR-215 has been implicated in the pathogenesis of several human malignancies, is upregulated in cervical cancer (10), hepatocellular carcinoma (11), gastric cancer (12) and prostate cancer (13) and acts as a potential oncogene in these tumors. [score:4]
Previous studies have confirmed that miR-215 is downregulated in esophageal adenocarcinoma (14), colon cancer (15) and RCC (16). [score:4]
ZEB2 is not the only miR-215 target dysregulated in NSCLC. [score:4]
The ZEB2 target was subsequently selected for further investigation as ZEB2 has been identified as an important oncogene in NSCLC (23) and a direct target of miR-215 in renal cell carcinoma (16). [score:4]
These data indicate that ZEB2 is a direct target of miR-215 in NSCLC. [score:4]
In conclusion, the results of the present study demonstrated that miRNA-215 was downregulated in NSCLC and correlated with aggressive clinicopathological features. [score:4]
In addition, downregulation of miR-215 reduced 95D cell apoptosis (Fig. 2C). [score:4]
Conversely, transfection of 95D cells with miR-215 inhibitors promoted cell invasion ability. [score:3]
In addition, a significant inverse correlation (R=−0.4216; P=0.0002) was observed between ZEB2 and miR-215 protein expression levels in NSCLC tumor tissues (Fig. 1E). [score:3]
In the present study, reduced miR-215 expression was identified in NSCLC specimens and cells and was correlated with aggressive clinicopathological features. [score:3]
Other functional targets of miR-215, including RB1 (35), TS (36), and ALCAM (37, 38), also modulate NSCLC pathogenesis. [score:3]
As demonstrated in Table I, miR-215 expression was significantly reduced in samples with lymph node metastasis (P=0.002) and advanced TNM stage (P<0.001). [score:3]
When the cells transfected with miR-215 mimics, miR-215 inhibitors or NC reached confluence, a scratch in the cell monolayer was made with a cell scratch spatula. [score:3]
ZEB2 and miR-215 expression are inversely correlated. [score:3]
ZEB2 is the target gene of miR-215. [score:3]
NSCLC cells (1×10 [6]; 100 µl cell suspension) stably overexpressing miR-215 or NC were inoculated subcutaneously into the mice (n=8 per group). [score:3]
To the best of our knowledge, the present study is the first to analyze the clinical significance and biological functions of miR-215 expression in NSCLC. [score:3]
In gastric cancer, increased miR-215 expression was significantly correlated with tumor invasion and ‘Union for International Cancer Control’ stage (12). [score:3]
In cervical cancer, miR-215 expression was significantly increased in the cancerous tissues of patients with lymph node metastasis, advanced ‘International Federation of Gynecology and Obstetrics’ tumor stage and poor survival (10). [score:3]
RT-qPCR analysis was performed to detect miR-215 expression in NSCLC tissues and cell lines. [score:3]
No significant differences were observed between miR-215 expression and age, gender, smoking status, cell types, T stage or tumor differentiation. [score:3]
miR-215 expression is associated with certain clinicopathological features of NSCLC. [score:3]
Subsequently, the cells were transfected with mature miR-215 mimics, miR-215 inhibitors (anti-miR-215), or negative control (miR-NC or anti-miR-NC) (Shanghai GenePharma Co, Ltd. [score:3]
Target searches for miR-215. [score:3]
Using the luciferase reporter assay, the present study demonstrated that ZEB2 was a direct target of miR-215 in NSCLC. [score:3]
These findings indicate that miRNA-215 may be a potential novel target for gene therapy of NSCLC. [score:3]
The overexpression of miRNA-215 exhibited anti-tumor effects in vitro and in vivo. [score:3]
Anti-miR-215 markedly inhibited the tumor growth of hepatoma cells in nude mice (11). [score:3]
Therefore, the potential regulatory circuitry affected by miR-215 is enormous, and the mechanisms underlying how miR-215 influences NSCLC progression require further clarification. [score:2]
As indicated in Fig. 4A–C, the tumors formed from miR-215 -overexpressing A549 cells were smaller and exhibited reduced tumor weights compared with those of the control tumors. [score:2]
As presented in Fig. 1A, the results demonstrated that the expression levels of miR-215 were significantly reduced in NSCLC specimens (8.2±1.9) compared with those in the corresponding adjacent non-cancerous tissues (19.2±4.0; P<0.001). [score:2]
The scratch migration assay also confirmed the inhibitory effect of miR-215 on NSCLC cell migration (Fig. 2E). [score:2]
However, to the best of our knowledge, the correlation between miR-215 expression and the clinicopathological characteristics of NSCLC has not previously been evaluated, and the biological roles of miR-215 and its direct functional targets in NSCLC remain poorly understood. [score:2]
In contrast to the aforementioned antitumor properties, miR-215 also functions as an oncogene in several types of cancer. [score:1]
In the present study, the expression of miR-215 and its clinical significance in NSCLC were evaluated. [score:1]
The associations between miR-215 expression and ZEB2 protein levels were evaluated using Pearson's correlation analysis. [score:1]
The effects of miR-215 on NSCLC cell phenotype were also analyzed. [score:1]
Previous studies have also demonstrated that miR-215 promotes the proliferation of hepatoma and gastric cancer cells (11, 12). [score:1]
The predicted binding of miR-215 with the ZEB2 3′UTR is illustrated in Fig. 3A. [score:1]
Flow cytometry was employed to determine the effect of miR-215 on cell apoptosis. [score:1]
Commercial lentiviral vectors containing miR-215 (LV-miR-215; Shanghai GeneChem Co. [score:1]
To further evaluate the effects of miR-215 on tumor growth in vivo, A549 cells were engineered to stably overexpress miR-215 by lentiviral infection. [score:1]
miR-215 influences the biological behaviors of NSCLC cells. [score:1]
All the reactions were performed in triplicate, and the 2 [−∆Ct] method (∆CT = CT [miR-215] − CT [U6]) was used to quantify the relative quantity of miR-215. [score:1]
miR-215, an identified p53 -induced miR, has been reported to be significant in the progression of cancer. [score:1]
org) were conducted using the search term ‘miR-215’. [score:1]
The results of the MTT assay demonstrated that cell proliferation was significantly impaired in A549 cells transfected with miR-215 mimics, while proliferation of 95D cells was enhanced following miR-215 inhibitors transfection, compared with that of the corresponding controls (Fig. 2B). [score:1]
Taken together, these findings indicate that the role of miR-215 in human malignancies may be multifaceted, depending on the specific tissue involved. [score:1]
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2
[+] score: 246
Downregulation of miR-215 expression also suppress gastric cancer cell invasion, and expression of miR-215 may be a potential biomarker for gastric cancer prognosis [25]. [score:10]
Downregulation of miR-215 expression suppresses gastric cancer cell invasion, suggesting the possibility that expression of miR-215 influences gastric cancer progression. [score:10]
These data indicate that CTNNBIP1 has high expression in adjacent normal tissue and low expression in tumor tissue; conversely miR-215 has high expression in tumor tissue and low in adjacent normal tissue. [score:7]
miR-215 was up-regulated in gastric cancer and prostate cancer using Taqman MicroRNA Assay [19– 23], although it was also down-regulated in other types of cancer [23– 25]. [score:6]
All these reports indicate that miR-215 exerts its biological and pathological function by regulating target gene expression. [score:6]
Importantly, it is reported that miR-215 is involved in the TGF-β1 -induced activation of the β-catenin pathway by directly targeting and decreasing expression of CTNNBIP1 [13]. [score:6]
For statistical analysis, miR-215 expression was divided into high and low expression groups (G4 versus G1–3). [score:5]
B. Comparison of 5-year progression free survival rate of glioma patients with high miR-215 expression with that of patients with low miR-215 expression. [score:5]
High miR-215 expression was detected in 90% (27/30) of glioma tissues and low miR-215 expression was detected in 100% (30/30) of adjacent normal tissue (Fig. 5C). [score:5]
Importantly, CTNNBIP1 expression is negatively correlated with miR-215 expression (r = −0.7893 95% CI −0.8691 to −0.6696; P < 0.0001) (Fig. 5C). [score:5]
miR-372, miR-21, mIR-10b, and miR-17 were intermediately expressed and 10 other miRNAs (miR-215, -34a, -124, -125b, -128, -137, -218, -326, -184, and -152) were lowly expressed in our cohort. [score:5]
miR-215 also inhibited the expression of BMP-6 through the BMP-6/miR-192 pathway to increase cell proliferation in breast cancer [34]. [score:5]
Additionally, the 5-year disease-free survival was lower in patients with overexpression of miR-215. [score:5]
Figure 3 A. The comparison of 5-year overall survival rate of glioma patients with high miR-215 expression with that of patients with low miR-215 expression. [score:5]
miR-215 decreases the expression of its targets, which include a number of cell cycle genes [29– 31]. [score:5]
We found that glioma patients with high miR-215 expression had a shorter median overall survival (OS) than those with low expression (44 months vs. [score:5]
Here, we observed that miR-215 was the most dramatically increased miRNA in human glioma and that the expression level of miR-215 is correlated with disease stage. [score:5]
A. The comparison of 5-year overall survival rate of glioma patients with high miR-215 expression with that of patients with low miR-215 expression. [score:5]
Overexpression of miR-215 reduced the expression of TYMS and MDM2 in renal cell carcinoma [33]. [score:5]
miR-215 was considered to be highly expressed if its relative expression level was ≥5. [score:4]
miR-215 is a positive regulator of Wnt/β-catenin signaling and prompts a TGF-β1 -induced increase of α-SMA and fibronectin specifically by suppression of CTNNBIP1 [12]. [score:4]
miR-215 is upregulated in gastric cancer and may be a potential biomarker for gastric cancer prognosis [11]. [score:4]
It is reported that CTNNBIP1 is a direct target of miR-215 [12]. [score:4]
These data indicate that miR-215 exerts its oncogenic and metastatic effect in the tumors by directly targeting CTNNBIP1 mRNA and mediating the TGF-β1 -induced activation of the β-catenin pathway in human glioma. [score:4]
miR-215 activates β-catenin pathways by decreasing TNNBIP1 expression in gliomas. [score:3]
We observed that high miR-215 expression is correlated with poor prognosis and advanced tumor stage in glioma patients. [score:3]
Figure 2 A. The expression level of miR-215 was higher in tumor tissues than in non-tumor tissues. [score:3]
Multivariate analysis using the same variables as in the univariate analysis in the cohort confirmed that miR-215 expression (P = 0.002, 95%CI HR 1.22–2.43), recurrence or metastasis (P = 0.01, 95%CI HR 2.29–4.16), and tumor dimension (P = 0.02, 95%CI HR 1.14–4.16) were independent poor prognostic parameters for glioma patients (Fig. 4B). [score:3]
miR-215 expression was greater in cervical tumors with vascular invasion and at FIGO (International Federation of Gynaecological Oncologists) stage. [score:3]
High miR-215 expression is a potential biomarker for diagnosis and prognosis in human glioma. [score:3]
Univariate analysis using the Cox proportional hazards mo del for all variables showed that high miR-215 expression (P = 0.001, 95%CI HR 1.32–2.63), recurrence or metastasis (P = 0.001, 95%CI HR 1.23–4.27), and tumor dimension (P = 0.003, 95%CI HR 1.24–2.66) were all independent poor prognostic parameters for glioma patients (Fig. 4A). [score:3]
The relation of miR-215 overexpression with the progression of cancer indicates its important role as an oncogene in cancer progression [22]. [score:3]
A. Univariate analysis of the hazard ratios for miR-215 overexpression, tumor dimension, and recurrence or metastasis as independent prognostic factors to predict the overall survival. [score:3]
High miR-215 expression is associated with poor prognosis in patients with gliomas. [score:3]
We observed that miR-215 is the most highly expressed miRNA in our cohort. [score:3]
Also, a correlation was observed between high miR-215 expression, tumor dimension, and tumor recurrence or metastasis (P = 0.012 and 0.042, respectively). [score:3]
High expression of miR-215 occurred more frequently in high-grade tumors (III–IV, 65.85%) than in low-grade tumors (I–II, 39.28%; P = 0.001). [score:3]
We also analyzed the correlation of CTNNBIP1 expression with that of miR-215. [score:3]
C. CTNNBIP1 mRNA and miR-215 expression levels in the tumor tissue and adjacent normal tissue are examined using qPCR and their correlation was analyzed by the Pearson correlation method. [score:3]
Here we examine miR-215 expression in human glioma and investigate the clinical significance of miR-215 overexpression. [score:3]
B. The expression levels of miR-215 in different stages of glioma. [score:3]
In summary, we identified that miR-215 is dramatically increased in human glioma and high miR-215 expression is correlated with poor prognosis, high tumor histologic grade, and advanced tumor progression. [score:3]
Indeed, we performed multivariate and univariate analysis in the cohort and showed that miR-215 expression, recurrence or metastasis, and tumor dimension were independent poor prognostic parameters for glioma patients. [score:3]
B. Multivariate analysis of the hazard ratios (HRs) for miR-215 overexpression, tumor dimension, and recurrence or metastasis as independent prognostic factors to predict the overall survival. [score:3]
Comparison of Kaplan-Meier survival curves for glioma patients in high and low miR-215 expression groups. [score:3]
miR-215 expression is increased in human glioma tissue. [score:3]
A. The expression level of miR-215 was higher in tumor tissues than in non-tumor tissues. [score:3]
We further examined miR-215 expression in 179 primary glioma and 20 non-neoplastic brain tissues by quantitative real-time PCR (qRT-PCR). [score:3]
No significant association of miR-215 expression was found with age, gender, or KPS score of the patients in the cohort (all P ≥ 0.05, Table 1). [score:3]
No significant difference in miR-215 expression was found between low-grade gliomas (WHO I and WHO II) (P = 0.068) (Fig. 2B). [score:3]
We observed a correlation between miR-215 expression and the histopathological grade (Table 1). [score:3]
To explore the effect of miRNAs on human gliomas, we measured the expression of miRNAs in human glioma tissue and found that miR-215 is the most highly expressed. [score:3]
The expression and function of miR-215 in human glioma tissues has yet to be explored. [score:3]
C. The expression level of miR-215 in WHO I+II and WHO III+IV stages of the glioma. [score:3]
miR-215 overexpression in glioma tissues as detected by qRT-PCR assay. [score:2]
MicroRNA-215 (miR-215), a transcript of chromosome 11q13.1, was initially thought to be a positive regulator of p53. [score:2]
miR-215 was also linked with the development, progression, and prognosis of prostate cancer [26– 28]. [score:2]
Expression of miR-215 was lower in low-grade gliomas (WHO I + II: 8.850 ± 0.30) compared to high-grade gliomas (WHO III + IV: 20.54 ± 0.39) (P < 0.001) (Fig. 2C). [score:2]
The gliomas were classified into 4 stages based on WHO criteria, and miR-215 expression was compared between the 4 stages of gliomas. [score:2]
Reports suggest that miR-215 may be a potential prognostic factor in cancer patients. [score:1]
We examined the association of miR-215 expression with clinicopathological characteristics in patients with gliomas. [score:1]
These data confirmed that miR-215 is a biomarker for clinical diagnosis and prognosis of human glioma. [score:1]
Tumor size was larger in nude mice injected with HeLa-miR-215 cells than in those injected with control cells [24]. [score:1]
All of these findings indicate that miR-215 is a marker for the poor prognosis of cervical cancer. [score:1]
We found increased levels of miR-215 in tumors with advanced staging (WHO I: 8.08 ± 0.52, WHO II: 9.24 ± 0.36, WHO III: 18.87 ± 0.58, WHO IV: 21.41 ± 0.50) (P < 0.001) (Fig. 2B). [score:1]
Furthermore, univariate and multivariate analyses for OS were performed to evaluate whether miR-215 expression levels and clinicopathological features were independent prognostic parameters of patient outcomes. [score:1]
miR-215 overexpression is associated with clinicopathological characteristics of human gliomas. [score:1]
miR-215 and miR-192 promoted apoptosis through the XIAP pathway in non-small cell lung cancer [35]. [score:1]
These data suggest that miR-215 not only has an oncogenic effect, but also can be a biomarker for diagnosis and prognosis of human glioma. [score:1]
Association between miR-215 expression and different clinicopathological characteristics of human gliomas. [score:1]
These data suggest the importance of miR-215 in glioma. [score:1]
These data indicate an important oncogenic role for miR-215 in human glioma. [score:1]
Levels of miR-215 in tumor tissues (16.88 ± 0.50) were higher than that in non-tumor tissues (3.06 ± 0.46) (P < 0.001) (Fig. 2A). [score:1]
These findings not only indicate the correlation of miR-215 with glioma progression, but also strongly suggest that it has an oncogenic effect. [score:1]
Next, we explored the mechanism underlying the oncogenic effect of miR-215. [score:1]
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3
[+] score: 78
Furthermore, we found a significant upregulation of miR-19, miR-192, miR-194, and miR-215 in the tumor compartment of the lung metastases and a significant downregulation of the same miRNAs in the liver metastases. [score:7]
In the host tissue of the liver metastases, we identified several miRNAs with significant correlations between expression and survival: downregulation of miR-125 (p = 0.05), miR-127 (p = 0.001), miR-145 (p = 0.005), miR-192 (p = 0.015), miR-194 (0.003), miR-199-5 (p = 0.008), miR-215 (p < 0.001), and miR-429 (p = 0.03) was associated significantly with poor survival (Table 4). [score:6]
miR-192 and miR-215 have been shown to be upregulated by p53, a tumor suppressor. [score:6]
Downregulation of miR-125 (p = 0.05), miR-127 (p = 0.001), miR-145 (p = 0.005), miR-192 (p = 0.015), miR-194 (p = 0.003), miR-199-5 (p = 0.008), miR-215 (p < 0.001), and miR-429 (p = 0.03) in the normal liver tissue was significantly associated with poor survival, suggesting oncosuppressive effects of these miRNAs. [score:6]
In the tumor stroma only miR-19, miR-215, and miR-21 showed a significant downregulation in the liver metastases compared to the lung metastases, but none of the miRNAs was downregulated more than by 2-fold. [score:6]
These contradictory results could be explained by the 1000-fold and 300-fold downregulation of miR-192, miR-194, and miR-215 in the host tissue of the lung compared to the liver, thus resulting in a relative upregulation in the tumor and stroma compartment. [score:6]
In the lung metastases miR-215 showed a 10-fold upregulation compared to the stroma and a 300-fold upregulation compared to normal lung tissue (p < 0.0001). [score:5]
miR-215 showed a 2.5-fold upregulation in the tumor compartment of the liver metastases compared to the stroma compartment (p < 0.0001) and no significant upregulation compared to the normal liver tissue. [score:5]
When combining the results of the expression of miRNAs in liver and lung metastases, only the expression of miR-145 and miR-215 in the host tissue was significantly associated with overall survival (p = 0.038 and p = 0.04, Figure 4). [score:5]
Our results show a downregulation of miR-192, miR-194, and miR-215 in the tumor and the tumor -associated stromal compartment of the liver metastases. [score:4]
Only three miRNAs, miR-127, miR-192, and miR-215, showed a significant expression difference (>2-fold) between all three compartments in both liver and lung metastases (Tables S1 and S2). [score:3]
Noteworthy, miR-215, miR-194, and miR-192 showed a more than 100-fold upregulation in the normal liver tissue compared to the normal lung tissue. [score:3]
miR-194 showed a 1.5-fold; miR-125, miR-127, and miR-192 showed a 2.5-fold; miR-19 and miR-215 a 3-fold; miR-145, miR-199-3, and miR-429 a 5-fold; miR-21 a 7-fold; and miR-199-5 a 12.5-fold downregulation in the liver metastases compared to the lung metastases. [score:3]
Especially miR-192, miR-194, and miR-215 were downregulated up to 350 times in the lung metastases compared to the liver metastases. [score:3]
miR-125 and miR-199-5 showed a 2-fold; miR-19 and miR-127 showed a 4-fold; miR-215 showed a 100-fold; miR-194 showed a 150-fold; and miR-192 showed a 300-fold upregulation in the normal liver tissue compared to the normal lung tissue. [score:3]
Georges S. A. Biery M. C. Kim S. Schelter J. M. Guo J. Chang A. N. Jackson A. L. Carleton M. O. Linsley P. S. Cleary M. A. Coordinated Regulation of Cell Cycle Transcripts by p53-Inducible microRNAs, miR-192 and miR-215 Cancer Res. [score:2]
Boni V. Bitarte N. Cristobal I. Zarate R. Rodriguez J. Maiello E. Garcia-Foncillas J. Bandres E. miR-192/miR-215 Influence 5-Fluorouracil Resistance through Cell Cycle-Mediated Mechanisms Complementary to Its Post-transcriptional Thymidilate Synthase Regulation Mol. [score:2]
The final selection of miRNAs for further analysis consisted of 11 miRNAs: miR-19b, miR-21, miR-125b, miR-127-3p, miR-145, miR-192, miR-194, miR-199a-3p, miR-199a-5p, miR-215, and miR-429. [score:1]
miR-192, -194 and -215 are located in the miR-215/miR-194-1 cluster on chromosome 1 (1q41) and the miR-192/miR-194-2 cluster on chromosome 11 (11q13.1). [score:1]
miR-194 and miR-215 are situated in the miR-215/miR-194-1 cluster on chromosome 1 (1q41). [score:1]
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4
[+] score: 47
B. Combined overview of three modules, including miR-215, miR-16, and 86 miR-215 targets and 191 miR-16 targets (21 targets in common). [score:7]
We found that targets in 2 out of 3 predicted modules were significantly down-regulated by the corresponding miRNAs, miR-16 and miR-215 (Figure 3). [score:6]
For example, miR-16 targets MAPK14 (p38 MAPK) and BID (also a miR-215 target), which are two key regulators in apoptosis -associated pathways [52, 53]. [score:6]
D. Heatmap showing down-regulation of miR-215 targets after transfection, similarly as in (B). [score:6]
C. Heatmap showing inverse expression patterns between miR-215 and its 86 targets (module #27 in Table 2), similarly as in (A). [score:5]
Both miRNAs targeted large number of genes, 191 for miR-16 and 86 for miR-215, and 21 genes were targeted by both (Figure 4A and 4B, module # 4, 27 and 28 in Table 2). [score:5]
In the protein interaction network, miR-16 and miR-215 targets interact with many other proteins, including targets of the same miRNA and another miRNA (Figure 4C). [score:5]
This sub-network suggests that HCV may be able to repress the expressions of several key genes in a number of HCV pathways via miR-16, miR-215, or both. [score:3]
Schema showing the relationships among module 4, 27, and 28 in Table 2. miRNAs are in red, and mRNA targets are in turquoise (miR-215), or in yellow (miR-215 and miR-16), or in green (miR-16). [score:3]
Out of 24 miRNAs studied, three of them, miR-16, miR-215 and miR-15b, happened to be in at least one of our predicted modules (Table 2). [score:1]
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5
[+] score: 34
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-22, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-127, mmu-mir-132, mmu-mir-133a-1, mmu-mir-136, mmu-mir-144, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-10b, mmu-mir-185, mmu-mir-190a, mmu-mir-193a, mmu-mir-203, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-10b, hsa-mir-34a, hsa-mir-203a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-144, hsa-mir-152, hsa-mir-127, hsa-mir-136, hsa-mir-146a, hsa-mir-185, hsa-mir-190a, hsa-mir-193a, hsa-mir-206, mmu-mir-148a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-22, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-337, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-29b-2, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-378a, mmu-mir-378a, hsa-mir-337, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-215, mmu-mir-411, mmu-mir-434, hsa-mir-486-1, hsa-mir-146b, hsa-mir-193b, mmu-mir-486a, mmu-mir-540, hsa-mir-92b, hsa-mir-411, hsa-mir-378d-2, mmu-mir-146b, mmu-mir-193b, mmu-mir-92b, mmu-mir-872, mmu-mir-1b, mmu-mir-3071, mmu-mir-486b, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, hsa-mir-203b, mmu-mir-3544, hsa-mir-378j, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-let-7k, hsa-mir-486-2
Down-regulated miRNAs Up-regulated target genes mmu-mir-148a ARL6IP1, ARPP19, ATP2A2, CCNA2, CSF1, EGR2, ERLIN1, ERRFI1, FIGF, GADD45A, GMFB, ITGA5, KLF4, KLF6, LIMD2, MAFB, NFYA, PDIA3, PHIP, PPP1R10, PPP1R12A, PTPN14, RAI14, RSBN1L, SERPINE1, SIK1, SLC2A1, TMEM127, TMSB10, TMSB4X mmu-mir-411 APOLD1, SPRY4 mmu-mir-136 RYBP, ARL10, GLIPR2, UGGT1 Up-regulated miRNAs Down-regulated target genes mmu-mir-34a/c DAB2IP, DMWD, EVI5L, FAM107A, MAZ, SPEG, TFRC, TTC19 mmu-mir-92b COL1A2, DAB2IP, G3BP2, HOXC11, LBX1, NFIX, PKDCC, PRKAB2 mmu-mir-132 ACTR3B, AMD1, GPD2, HBEGF, KBTBD13, KCNJ12, PRRT2, SREBF1, TLN2 mmu-mir-146a IRAK1, TLN2 mmu-mir-152 EML2, GPCPD1, NFIX, RPH3AL, SH3KBP1, TFRC, TRAK1, UCP3 mmu-mir-155 DUSP7, G3BP2 mmu-mir-185 DAB2IP, FAM134C, SYNM, TMEM233 mmu-mir-203 APBB2, CACNG7, FKBP5, GDAP1, HBEGF, KCNC1, SIX5, TMEM182 mmu-mir-206 DMPK, G3BP2, GPD2, KCTD13, MKL1, SLC16A3, SPEG mmu-mir-215 KLHL23 Figure 5The network displays the predicted interactions between age-related miRNAs and mRNAs from the sequencing and was generated using Cytoscape (version 3.0, www. [score:17]
Down-regulated miRNAs Up-regulated target genes mmu-mir-148a ARL6IP1, ARPP19, ATP2A2, CCNA2, CSF1, EGR2, ERLIN1, ERRFI1, FIGF, GADD45A, GMFB, ITGA5, KLF4, KLF6, LIMD2, MAFB, NFYA, PDIA3, PHIP, PPP1R10, PPP1R12A, PTPN14, RAI14, RSBN1L, SERPINE1, SIK1, SLC2A1, TMEM127, TMSB10, TMSB4X mmu-mir-411 APOLD1, SPRY4 mmu-mir-136 RYBP, ARL10, GLIPR2, UGGT1 Up-regulated miRNAs Down-regulated target genes mmu-mir-34a/c DAB2IP, DMWD, EVI5L, FAM107A, MAZ, SPEG, TFRC, TTC19 mmu-mir-92b COL1A2, DAB2IP, G3BP2, HOXC11, LBX1, NFIX, PKDCC, PRKAB2 mmu-mir-132 ACTR3B, AMD1, GPD2, HBEGF, KBTBD13, KCNJ12, PRRT2, SREBF1, TLN2 mmu-mir-146a IRAK1, TLN2 mmu-mir-152 EML2, GPCPD1, NFIX, RPH3AL, SH3KBP1, TFRC, TRAK1, UCP3 mmu-mir-155 DUSP7, G3BP2 mmu-mir-185 DAB2IP, FAM134C, SYNM, TMEM233 mmu-mir-203 APBB2, CACNG7, FKBP5, GDAP1, HBEGF, KCNC1, SIX5, TMEM182 mmu-mir-206 DMPK, G3BP2, GPD2, KCTD13, MKL1, SLC16A3, SPEG mmu-mir-215 KLHL23 Figure 5The network displays the predicted interactions between age-related miRNAs and mRNAs from the sequencing and was generated using Cytoscape (version 3.0, www. [score:17]
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6
[+] score: 31
miR-192 and miR-215 have been shown to be dramatically upregulated and are involved in promoting renal glomerular and tubulointerstitial fibrosis in DN [9]. [score:4]
In our study, we found that exposure to high glucose increased the expression of EV miR-192 and miR-215 in HK-2. In addition, we also determined that miR-192 expression was higher in HK-2 EVs compared to the other two miRNAs as we found in urine samples. [score:4]
miR-192, miR-194, and miR-215 have been reported to be highly expressed in kidney tissue and play critical roles in kidney development and differentiation [7]. [score:4]
We found that exposure to high glucose significantly enhanced EV miR-192 (t = 7.129, P = 0.019), miR-194 (t = 4.008, P = 0.016), and miR-215 (t = 4.806, P = 0.04) expression levels in HK-2 cells (Figure 5). [score:3]
The expression of urinary EV miR-192, miR-194, and miR-215 was increased in T2DM patients with microalbuminuria. [score:3]
As we expected, TGF- β1 levels were positively correlated with both miR-192 (r = 0.356, P = 0.005) and miR-215 (r = 0.332, P = 0.010). [score:1]
In EVs from hMCs, no significant differences were found between miR-192 and either miR-194 (t = 1.333, P = 0.212) or miR-215 (t = 1.146, P = 0.278) (Figure 6). [score:1]
There was no significant difference between miR-194 and miR-215 (Z = 0.452, P = 0.651). [score:1]
In our study, these miRNAs were also detected in urinary EVs, and the relative abundance of miR-192 was significantly higher than those of miR-194 (Z = 7.913, P < 0.001) and miR-215 (Z = 8.405, P < 0.001), which suggests that miR-192 plays a more important role in the DN process, specifically in renal cell communication. [score:1]
In addition, in EVs from HK-2 cells from both the NG and the HG groups, the miR-192 levels were significantly higher than those of miR-194 (t = 3.001, P = 0.03) and miR-215 (t = 2.668, P = 0.043). [score:1]
Levels of miR-192 (Z = 3.777, P < 0.001), miR-194 (Z = 2.210, P = 0.027), and miR-215 (Z = 3.046, P = 0.002) in patients with diabetes with microalbuminuria were higher than those with normoalbuminuria. [score:1]
miR-215 and miR-194-1 are located on the same chromosome, as are miR-192 and miR-194-2. miR-192 and miR-215 share the same seed sequence, and miR-194-1 and miR-194-2 possess the same mature sequence [8]. [score:1]
TGF- β1 levels were significantly correlated with miR-192 (r = 0.356, P = 0.005) and miR-215 (r = 0.332, P = 0.010), and no significant correlation was detected between TGF- β1 levels and miR-194 (r = 0.190, P = 0.146) (Figure 4). [score:1]
No correlation was found with miR-194 (r = 0.164, P = 0.211) and miR-215 (r = 0.250, P = 0.054). [score:1]
miR-192, miR-194, and miR-215 are particularly abundant in the kidneys relative to other organs [7]. [score:1]
ROC analysis revealed that miR-192 had an area under the curve (AUC) of 0.802 (95% confidence interval, 0.696–0.907, P < 0.001), which was better than miR-194 with an AUC of 0.703 (95% confidence interval, 0.581–0.826, P = 0.04) and miR-215 with an AUC of 0.757 (95% confidence interval, 0.545–0.869, P < 0.001) in discriminating the normoalbuminuric group from the microalbuminuric group (Figure 3). [score:1]
As shown in Table 2, miR-192 levels were higher than the levels of miR-194 (Z = 7.913, P < 0.001) and miR-215 (Z = 8.405, P < 0.001) in urinary EVs. [score:1]
Indeed, miR-192 and miR-194 are highly enriched in proximal tubule and mesangial cells [28], and miR-192 and miR-215 have been shown to play roles in mesangial cell hypertrophy and fibrogenesis [9, 42]. [score:1]
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7
[+] score: 28
Hsa-miR-215 mediated targets/pathways based on translational immunoprecipitation expression analysis [30], and the CDX1–miR-215 axis seem to regulate CRC stem cell differentiation [31]. [score:8]
A strong correlation was observed for hsa-miR-378a (Pearson’s r = 0.9), hsa-miR-375 (r = 0.77) and hsa-miR-215-5p (r = 0.75), underlining that Illumina sequencing is a useful and correct tool for this screen while TaqMan PCR can be regarded as a quick and inexpensive way to determine the expression of a single miRNA. [score:3]
Four miRNAs were selected based on lowest P [adj] values and mean expression levels: hsa-miR-21-5p, hsa-miR-215-5p, hsa-miR-375 and -378a. [score:3]
Hsa-miR-215 is associated with inhibition of CRC relapse following radical surgery [34]. [score:3]
Thus, rectal and colon cancers associate with specific miRNA deregulation, specifically of hsa-miR-21-5p, hsa-miR-215-5p, and hsa-miR-378a. [score:2]
Details are listed in Supplementary Table 1. Strikingly, the DESeq2 calculation revealed a highly significant upregulation (P [adj] < 0.00001) of three miRNA molecules in both colon as well as rectal cancer: hsa-miR-21-5p, hsa-miR-378a, and hsa-miR-215-5p. [score:2]
In addition, we demonstrated that a small group among more than 1850 miRNA molecules, i. e. hsa-miR-378a, hsa-miR-21-5p, and hsa-miR-215-5p, are of special interest for CRC detection and may have predictive potential. [score:1]
The results of the correlation are visualized as bar diagrams on the left and scatter diagrams with regression lines on the right comparing next generation sequencing (blue/y-axis) and TaqMan fold changes (red/x-axis) for hsa-miR-378a (A), hsa-miR-375 (B), hsa-miR-21-5p (C) and hsa-miR-215-5p (D). [score:1]
Three miRNA molecules were highly sensitive and specific for detecting CRC: hsa-miR-378a, hsa-miR-215-5p, and hsa-miR-21-5p. [score:1]
We selected three microRNAs miR-21-5p (AUC 0.79, 95% CI 0.70–0.88), miR-215-5p (AUC 0.83, 95% CI 0.76–0.91) and miR-378a (AUC 0.84, 95% CI 0.76–0.92) which were the most promising candidates for colorectal cancer. [score:1]
An evaluation and replication of miRNAs with disease stage and CRC-specific mortality have also been shown for hsa-miR-215 [32, 33]. [score:1]
Our data further identified an important role for hsa-miR-215-5p in colon as well as rectal cancer. [score:1]
There was a good correlation of the NGS with the TaqMan results with a strong relationship for hsa-miR-378a (Pearson’s r = 0.9), hsa-miR-375 (r = 0.77) and hsa-miR-215-5p (r = 0.75), but only a moderate relationship for hsa-miR-21-5p (r = 0.53). [score:1]
[1 to 20 of 13 sentences]
8
[+] score: 26
The expression of miR-215-5p, miR-199a-5p & 3p was analyzed by real-time PCR and Northern blot (Fig. 7C–F), demonstrating that the induction of miR-215, miR-199a-5p&3p after UUO was inhibited in PT-p53- KO mice. [score:5]
Previous results demonstrated that p53 directly induced miR-215 expression 33, which is known to be involved in increased collagen production and the progression of diabetic nephropathy by regulating the CTNNBIP1/β-catenin pathway 20. miR-199a-5p (previously called miR-199a) and miR-199a-3p (previously called miR-199a*) are two mature forms derived from the same precursor in the human genome 34 35. [score:5]
The expressions of three miRNAs, miR-215-5p and miR-199a-5p&3p, were found to be consistently high in wide type mice with UUO, and they were decreased in renal cortex of global p53 knockout mice with UUO. [score:4]
However, the two down-regulated miRNAs, miR-215-5p and miR-199a-5p were correlated with the amelioration of renal fibrosis 20 21. [score:4]
The induction of miR-215, miR-199a-5p, and miR-199a-3p after UUO was suppressed in PT-p53- KO mice. [score:3]
The induction of miR-215, miR-199a-5p&3p after UUO was suppressed in PT-p53- KO mice. [score:3]
Total RNA (10 μg per lane) was analyzed by Northern blotting as described in the concise Methods section using a [32]p-labeled probe of miR-215, miR-199a-5p, and miR-199a-3p. [score:1]
Previous studies have demonstrated that both miR-215-5p and miR-199a-5p were related to the renal fibrosis 20 21, hence, we focused on the miR-199a-3p. [score:1]
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9
[+] score: 25
Other miRNAs from this paper: hsa-mir-21, hsa-mir-192, hsa-mir-221, hsa-mir-222
In addition, the identification of the long 3′ UTR of human IL-21 mRNA and transfection studies revealed that human IL-21 mRNA with the long 3′ UTR is down-regulated by miR-21, miR-192, miR-215, miR-221, and miR-222, which were in the top 25 miRNAs up-regulated by. [score:7]
Collectively, the present study is the first demonstration that human IL-21 mRNA is down-regulated by miR-21, miR-192, miR-215, miR-221, and miR-222, suggesting a novel regulatory mechanism of IL-21 expression in immune responses. [score:7]
Previously the expression of miR-21, miR-221, and miR-222 was reported to be increased in EVs from patients infected with HBV 24, 25 and miR-215 was also shown to increase in the serum derived from patients infected with HBV [37]. [score:3]
s revealed that miR-21, miR-192, miR-215, miR-221, and miR-222 repressed the expression of the reporter gene with the long 3′ UTR of human IL-21 mRNA (Fig.   3A). [score:3]
In this study, we have shown that the expression of human IL-21 in T cells was repressed by transduction of miR-21, miR-192, miR-215, miR-221, and miR-222. [score:3]
In the long 3′UTR of human IL-21 cDNA we identified, there are multiple conserved miRNA binding sites for miR-21, miR-192, miR-215, miR-221, and miR-222, (Fig.   2D and Fig.   S4). [score:1]
Interestingly, it was reported that miR-21, miR-192, miR-215, miR-221, and miR-222 were enriched in exsosomes derived from sera of cancer patients and supernatants of cancer cells 42– 47. [score:1]
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10
[+] score: 25
To assess the reliability of our selected RGs, we performed a target analysis on miR-215-5p, previously found to be up-regulated in CHB in children and adults as well as in HBV-related HCC [14, 23, 24, 39]. [score:6]
Liu F You X Chi X Wang T Ye L Niu J Hepatitis B virus X protein mutant HBxDelta127 promotes proliferation of hepatoma cells through up -regulating miR-215 targeting PTPRTBiochemical and biophysical research communications. [score:4]
We also normalised against the commonly used RG U6 and found miR-215-5p to be up-regulated by 11.2 fold (p = 0.01). [score:4]
We found a significant up-regulation of miR-215-5p in the DOXY cell line compared to the control HepG2 tet-on cell line (0.2 fold, p = 0.04). [score:3]
The optimal set of reference genes was verified by a target analysis using RT-qPCR on miR-215-5p. [score:3]
We studied the expression of miR-215-5p in HepG2 cells with and without HBV replication by RT-qPCR after 48 h of doxycycline treatment, and we normalised using miR-24-3p, miR-151a-5p, and miR-425-5p. [score:3]
We identified miR-24-3p, miR-151a-5p, and miR-425-5p as the most valid combination of RGs to use for microRNA studies in this HBV-replicating HepG2 cell system and confirmed their validity with miR-215-5p. [score:1]
were verified by assessment of miR-215-5p, which is known to have a role in the pathogenesis of HBV infection [23, 24]. [score:1]
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11
[+] score: 23
Identification of miR-215 mediated targets/pathways via translational immunoprecipitation expression analysis (TrIP-chip). [score:7]
Although the miRNAs discussed in this section are oncogenic, both miR-215 (Chiang et al., 2012; Karaayvaz et al., 2011; Faltejskova et al., 2012; Slattery et al., 2015) and miR-375 (Dai et al., 2012; Faltejskova et al., 2012; Wang et al., 2014d; Xu et al., 2014, 2016) are tumor-suppressive miRNAs that could be used for CRC screening, although an analysis of miRNA levels in blood or stool is needed. [score:3]
Dicer (Iliou et al., 2014) and multiple miRNAs [including, miR-34a (Bu et al., 2013, 2016), miR-106b (Zheng et al., 2015a), miR-140 (Zhai et al., 2015), miR-146a (Hwang et al., 2014), miR-183 (Wellner et al., 2009), miR-200 (Wellner et al., 2009), miR-203 (Wellner et al., 2009), miR-215 (Jones et al., 2015), miR-302b (Zhu et al., 2012), miR-328 (Xu et al., 2012b), miR-363 (Tsuji et al., 2014), miR-371 (Li et al., 2015c) and miR-451 (Bitarte et al., 2011)] reportedly regulate CRC TICs. [score:2]
MiR-215 (and the related miR-192), functions in part by regulating cell cycle genes and by repressing cell proliferation (Boni et al., 2010; Fesler et al., 2015; Jones et al., 2015). [score:2]
MicroRNA-215 inhibits relapse of colorectal cancer patients following radical surgery. [score:2]
miR-192/miR-215 influence 5-fluorouracil resistance through cell cycle -mediated mechanisms complementary to its post-transcriptional thymidilate synthase regulation. [score:2]
The CDX1-microRNA-215 axis regulates colorectal cancer stem cell differentiation. [score:2]
Prognostic significance of miR-215 in colon cancer. [score:1]
This is consistent with the prognostic features of miR-192 (Chiang et al., 2012) and miR-215 (Karaayvaz et al., 2011; Faltejskova et al., 2012; Chiang et al., 2012; Li et al., 2013b), which are both depleted in CRC tumors. [score:1]
Conversely, miR-215, which is transcriptionally activated by the intestinal-specific transcription factor CDX1, appears to repress stem cell markers and is significantly depleted in CRC TICs (Jones et al., 2015). [score:1]
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12
[+] score: 22
It was shown that miR-192, miR-194 and miR-215 are highly expressed in normal colon tissue while their expression is dramatically decreased in colon cancer. [score:5]
Consequently, increased expression of miR-194 and miR-215 in duodenum and proximal jejunum are probably involved in promoting epithelial differentiation in order to replace cells that differ e. g. in transport functions. [score:3]
Consistently, in distal parts of the intestine we determined diminished expression of miR-194 and miR-215, respectively pointing to a higher proliferative activity in the distal parts. [score:3]
In our microarray experiments, miR-194 and miR-215 showed the same expression pattern along the entire intestine, underlining the fact that both may derive from one transcript. [score:3]
Cluster I (Figure 3E) shown in the hierarchically clustered heatmap harbored only miR-194 and miR-215, which were highly expressed in the proximal parts of the small intestine (duodenum and proximal jejunum). [score:3]
Interestingly, miR-194 and miR-215 were both duplicated and located on chromosomes X and 10 and clustered within a 353 bp chromosomal region. [score:1]
A) ssc-miR-215, B) MDM238, C) MDM392, D) ssc-miR-30a, E) ssc-miR-194, F) ssc-miR-374b, G) ssc-miR-155, H) ssc-miR-4331. [score:1]
We have identified several genomic clusters one of those including the porcine miRNAs miR-194 and miR-215. [score:1]
They identified two genomic clusters in the human genome either encoding miR-194-1 and miR-215 on chromosome 1 or encoding miR-194-2 and miR-192 on chromosome 11 [30]. [score:1]
In contrast to human, both porcine clusters are 100% identical encoding only miR-194 and miR-215. [score:1]
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13
[+] score: 19
Another study that compared select miRNA between paired squamous and columnar tissues from seven BE patients found miR-215 and -192 to be upregulated and miR-203 and -205 to be downregulated in the columnar epithelium [46]. [score:6]
miR-215 that was highly expressed in human BE tissues was expressed only in the BAR-T cell line, perhaps suggesting BAR-T to be a good cell line for biological experiments of miRNA modulation to further understand the pathways associated with BE pathogenesis. [score:5]
miR-215 that was highly expressed in human BE tissues was expressed only in the BAR-T cell line. [score:5]
Our NGS dataset not only confirmed the significantly different expression of miR-215, -192, -203 and -205 between GERD and BE but took a more comprehensive approach to identify several novel miRNA not previously described in BE, such as miR-708, -944, -224-5p, -3065-5p among others. [score:3]
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14
[+] score: 18
Although we observed upregulation of miR-143 and miR-145 in squamous mucosa from individuals with ulcerative oesophagitis, we did not observe altered expression of other miRNAs, miR-21, miR-194 and miR-215, which have previously been shown to be increased in Barrett’s oesophagus mucosa. [score:6]
miR-203 and miR-205 are expressed at higher levels in squamous mucosa, and miR-143, miR-145, miR-194 and miR-215 are expressed at higher levels in Barrett’s oesophagus. [score:5]
Previous work from our laboratory which compared normal squamous oesophageal mucosa with Barrett’s oesophagus showed increased expression of miR-21, miR-143, miR-145, miR-194 and miR-215, and decreased expression of miR-203 and miR-205 in Barrett’s oesophagus. [score:4]
There were no significant differences between the 2 groups of squamous mucosae for the expression of miR-21, miR-194, miR-203 and miR-215. [score:3]
[1 to 20 of 4 sentences]
15
[+] score: 18
Expression of WT TP53 in TP53-mutant H1299 resulted in miR-192-5p and miR-215 expression after CUR treatment. [score:5]
These studies revealed that the X-linked inhibitor of apoptosis (XIAP) was a novel transcription target of miR-192-5p and miR-215 in non-small cell lung cancer [165]. [score:5]
miR-192-5p and miR-215 functioned as tumor suppressors in these cells. [score:3]
The effects of CUR were shown to be dependent on miR-192-5p and miR-215 expression. [score:3]
CUR activated both miR-192-5p and miR-215 in TP53 WT A427 cells. [score:1]
CUR has been shown to activate the TP53/miR-192-5p/miR-215/XIAP pathway in NSCLC. [score:1]
[1 to 20 of 6 sentences]
16
[+] score: 17
Reduced expression of miR-192, miR-215 and miR-10b in liver samples of rat from fish oil group (Fig. 3B) resulted in a de-repression of their targets plasminogen activator inhibitor type 1 (Serpine1) and insulin-like grow factor 2 (Igf2), as both genes have predicted binding sites for these three miRNAs. [score:7]
Among the validated gene targets of some of these miRNAs, there is the insulin grown factor pathway (Igf-1r and Igf-1), which is targeted by miR-192 and miR-215 [33]. [score:5]
Similarly, miR-215 expression decreased after FO compared to OO and PO diets and miR-26b-5p expression decreased after FO compared with PO diet and miR-9a-5p after FO compared with SO diet. [score:2]
Compared to all other treatments, miR-215 expression was significantly induced by FO consumption, while miR-10b and miR-9a were induced by LO (Fig. 3A). [score:2]
Likewise, we observed a decrease in the expression of several hepatic miRNAs, namely miR-192–5p, miR-10b-5p, miR-377–3p, and miR-215 after FO compared with OO and PO diets and miR-21–5p and mir-26b-5p after FO compared with PO diets. [score:1]
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17
[+] score: 17
Chau and colleagues [28] showed that genotoxic stress could lead to up-regulation of miR-192 and miR-215, which in turn lead to a gene expression signature that is highly enriched for regulators of cell cycle. [score:7]
Therefore, factors other than p53 are responsible for the increase in miR-192 and miR-215 expression level. [score:3]
These results imply that miR-192 and miR-215 work in synergy with the p53 pathway in regulating cell cycle arrest and thus they are critical to tumor formation. [score:2]
miR-192 and miR-215 Induces p53-Mediated Cell Cycle Arrest. [score:1]
Thus, miR-192, miR-194 and miR-215 are regarded as an amplifier to p53 and p53 -dependent mediators of cell cycle arrest. [score:1]
In a recent paper published by Dobbelstein and colleagues [26] p53 was shown to induce, together with miR-34a, three additional miRNAs: miR-192, miR-194, and miR-215. [score:1]
The miR-34 story set the precedence and a number of papers have now been published showing that other miRNAs interfere the p53 pathway, in a p53-independent manner (miR-34), partial p53 -dependent manner (miR-192, miR-194, miR-215, and miR-21) or a p53 -dependent manner (miR-29). [score:1]
Furthermore, miRNAs is implicated in every aspect of cellular outcome of p53 activation: apoptosis (miR-34 and miR-29), cell cycle arrest (miR-192, miR-194, and miR-215), and senescence (miR-34). [score:1]
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18
[+] score: 15
Therefore, downregulation of miR-215 could promote EMT phenotype in downregulation of E-cadherin and promote EMT phenotype in the cycling hypoxia-selected subpopulation. [score:7]
miR215 suppresses EMT by suppressing the mesenchymal transcription factor ZEB2 and increasing the E-cadherin level [39]. [score:5]
In addition to miRNA200c and miR205, the cycling hypoxia-selected subpopulation showed decreased miR215 expression (Figure 6e). [score:3]
[1 to 20 of 3 sentences]
19
[+] score: 15
And mir-215, which has been shown to have reduced expression in cancer tissues compared to normal cells, is capable of inducing cell-cycle arrest, colony suppression and cell detachment from a solid support when transfected into cells [44]. [score:4]
Five of the twenty snoRNA-like miRNAs, mir-664, mir-151, mir-605, mir-215 and mir-140 were selected for this analysis because they are expressed in HeLa cells. [score:3]
We tested the predictions by experimentally showing that the precursors of five of the predicted snoRNA-like miRNAs, mir-664, mir-151, mir-605, mir-215 and mir-140, interact with dyskerin, a protein component of functional H/ACA snoRNPs. [score:1]
Screenshots of the UCSC Genome Browser [48] displaying RefSeq genes (blue lines with hatch marks), miRNA hairpins (red blocks), snoRNAs (green blocks with hatch marks), repeat-elements (blue blocks with hatch marks) and TSDs (black blocks) are shown for the genomic regions surrounding mir-215 (A), mir-549 (B), mir-1266 (C) and mir-605 (D). [score:1]
Apart from the predicted snoRNAs that contain mir-151 and mir-215, all predicted snoRNAs in Table 2 contain at least 90% of their encoded miRNA hairpins. [score:1]
Of the five extended miRNA regions that we experimentally found to be bound by dyskerin, three (mir-151, mir-140 and mir-215) have been further characterized and functionally validated, either by studies of their processing into their mature form or validation of their targets and effects. [score:1]
Only two (mir-215 and mir-140) of our twenty miRNAs encoded in predicted snoRNAs are classified as protypical in this study. [score:1]
1000507.g004 Figure 4Screenshots of the UCSC Genome Browser [48] displaying RefSeq genes (blue lines with hatch marks), miRNA hairpins (red blocks), snoRNAs (green blocks with hatch marks), repeat-elements (blue blocks with hatch marks) and TSDs (black blocks) are shown for the genomic regions surrounding mir-215 (A), mir-549 (B), mir-1266 (C) and mir-605 (D). [score:1]
C RT-PCR used to detect co-precipitated hsa-mir-664, hsa-mir-151, hsa-mir-605, has-mir-215 and has-mir-140 miRNA precursors, with E2 box H/ACA snoRNA as positive control and hsa-pri-let-7g miRNA, U3 box C/D snoRNA, U1 snRNA, 5S rRNA and GAPDH pre-mRNA as negative controls for dyskerin -associated RNAs. [score:1]
Approximately 80% of the hairpins of both mir-151 and mir-215 are contained in their respective predicted snoRNA. [score:1]
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[+] score: 15
Su et al. (2015) demonstrated that miR-181a inhibits differentiation of HL-60 cells and CD34+ hematopoietic stem/progenitor cells by directly targeting PRKCD-P38-C/EBPα pathway [59] and Jones et al. (2015) reported that miR-215 target caudal-type homeobox 1 (CDX1) and regulates colorectal cancer stem cell differentiation [60]. [score:9]
The above mentioned miRNAs (miR-371b-5p, miR-181a and miR-215) were up-regulated with treatment of vitamin C to hBMSCs. [score:4]
Jones M. F. Hara T. Francis P. Li X. L. Bilke S. Zhu Y. Pineda M. Subramanian M. Bodmer W. F. Lal A. The CDX1-microRNA-215 axis regulates colorectal cancer stem cell differentiationProc. [score:2]
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[+] score: 13
Other miRNAs from this paper: hsa-let-7d, hsa-mir-107, hsa-mir-224, hsa-mir-15b, hsa-mir-324
They identified induction of cyclin -dependent kinase inhibitor 1A (p21) as a common target of urolithins and could link p21 induction with downregulation of onco-miR-224 or upregulation of tumour suppressor miR-215 [45]. [score:13]
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[+] score: 13
The expression of miR-221, miR-18a, miR-18b, and miR-423-5p in poorly differentiated HCC were significantly higher than in well differentiated HCC, and 8 miRNAs (miR-455-3p, miR-1914*, miR-100, miR-215, miR-122*, let-7b, miR-22 and miR-99a) in poorly differentiated HCC had significantly lower expression levels than in well differentiated HCC (p < 0.05) (Table  2). [score:5]
14.0 and showed that the expression of miR-221, miR-18a, miR-18b, and miR-423-5p in poorly differentiated HCC were significantly higher than in well differentiated HCC, and 8 miRNAs (miR-455-3p, miR-1914*, miR-100, miR-215, miR-122*, let-7b, miR-22 and miR-99a) in poorly differentiated HCC were expressed significantly lower than in well differentiated HCC. [score:5]
Homo sapiens trinucleotide repeat containing 6B (TNRC6B) was a common hypothetical target gene in miR-221, miR-18a, miR-18b, miR-423-5p, miR-455-3p, miR-1914*, miR-215, miR-122*, let-7b, and miR-22 using miRanda algorithm. [score:3]
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[+] score: 12
In detail, the expression of miR-186, miR-215 and miR-223 resulted upregulated in ATRA differentiated cells, while the expression of miR-17-5p, miR-25, miR-193, miR-195, and let-7a resulted downregulated (the miRNAs bolded were already reported as deregulated by ATRA in differentiated NB4 cells in refs. [score:12]
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[+] score: 12
miR-215 promotes cell migration and invasion of gastric cancer cells, and acts as an oncogene in high-grade glioma by regulating retinoblastoma 1 42, 43, even though, it suppresses proliferation and migration of non-small cell lung cancer cells and epithelial ovarian cancer cells 44, 45. miR-150 is downregulated in osteosarcoma and suppresses cell proliferation, migration, and invasion [46]. [score:9]
Thus, we observed some miRNAs, such as hsa-miR-3127-3p, hsa-miR6756-3p, hsa-miR150-5p, and hsa-miR215-5p, with proportions below 100, which regulated the Hh pathway to a greater extent. [score:2]
Our data shows that hsa-miR-29a, hsa-miR-3127, hsa-miR-375, hsa-miR-6756, hsa-miR-335, hsa-miR-92a, hsa-miR-150, hsa-miR-215, hsa-miR-155, hsa-miR-193b, hsa-miR-24, and hsa-miR-149 are strong candidates for further studies on the Hh signaling pathway in ADSCs. [score:1]
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25
[+] score: 11
In human fibrotic disease, miRNA-215 suppresses fibroblast proliferation by targeting ASK1; several miRNAs targeting ASK1 were introduced as new therapeutic targets for kidney fibrosis [37, 38]. [score:11]
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[+] score: 11
5) 7 hsa-mir-19a dbDEMC 32 hsa-mir-30d dbDEMC 8 hsa-mir-92a HMDD, miR2Disease 33 hsa-mir-451 literature 9 hsa-mir-210 miR2Disease 34 hsa-mir-152 dbDEMC 10 hsa-mir-19b dbDEMC, miR2Disease 35 hsa-mir-215 dbDEMC 11 hsa-mir-224 dbDEMC, miR2Disease 36 hsa-mir-130a dbDEMC, HMDD 12 hsa-let-7f dbDEMC, miR2Disease 37 hsa-mir-499 higher RWRMDA (No. [score:11]
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[+] score: 10
Wang et al. have suggested that overexpression of miR-215 in HCC cells is correlated with upregulated chemoresistance, via targeting of dihydrofolate reductase (DHFR) and thymidylate synthase, and proliferation, via effects on P21 expression [15]. [score:10]
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[+] score: 10
severe (p<0.05) cfa-let-7d, cfa-miR-101, cfa-miR-10a, cfa-miR-1296, cfa-miR-1306, cfa-miR-1307, cfa-miR-130a, cfa-miR-136, cfa-miR-17, cfa-miR-181b, cfa-miR-196b, cfa-miR-197, cfa-miR-215, cfa-miR-22, cfa-miR-30d, cfa-miR-33b, cfa-miR-497, cfa-miR-503, cfa-miR-574, cfa-miR-628, cfa-miR-676Comparing the miRNA differential expression analyses between disease states obtained by RT-qPCR and RNAseq, we observed discordances between the two methods. [score:5]
severe (p<0.05) cfa-let-7d, cfa-miR-101, cfa-miR-10a, cfa-miR-1296, cfa-miR-1306, cfa-miR-1307, cfa-miR-130a, cfa-miR-136, cfa-miR-17, cfa-miR-181b, cfa-miR-196b, cfa-miR-197, cfa-miR-215, cfa-miR-22, cfa-miR-30d, cfa-miR-33b, cfa-miR-497, cfa-miR-503, cfa-miR-574, cfa-miR-628, cfa-miR-676 Comparing the miRNA differential expression analyses between disease states obtained by RT-qPCR and RNAseq, we observed discordances between the two methods. [score:5]
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[+] score: 10
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7e, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-20a, hsa-mir-21, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-101-1, hsa-mir-106a, hsa-mir-107, hsa-mir-192, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-214, hsa-mir-222, hsa-mir-223, hsa-mir-1-2, hsa-mir-15b, hsa-mir-125b-1, hsa-mir-141, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-149, hsa-mir-184, hsa-mir-186, hsa-mir-200c, hsa-mir-1-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-339, hsa-mir-146b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-624, hsa-mir-650, hsa-mir-651, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-449b, hsa-mir-1185-2, hsa-mir-1283-1, hsa-mir-1185-1, hsa-mir-708, hsa-mir-548e, hsa-mir-548j, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-1283-2, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
An overall down-regulation of the Rb pathway was apparent, with mutations in RB1 in three samples and global up-regulation of MDM2 (RB1 repressor) and of RB1 -targeting miRNAs (miR-215, miR-106a, miR-17, miR-20a, miR-93, miR-215, miR-21). [score:10]
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IsomiRs in other tissues such as isomiRs of miR-215 in the intestine (Additional file 11: Figure S3), miR-192-5p in the liver (Additional file 12: Figure S4) and miR-3473f-pre in the testis (Additional file 13: Figure S5 and Additional file 14: Figure S6) display similar isomiR expression. [score:3]
IsomiRs of miR-215 display more expanded or restricted expression with respect to tissues. [score:3]
Eli Lilly investigated the isomiR expression of pancreas tissue specific and enriched miRNAs and the analysis revealed that isomiRs generally mirror their parent miRNA expression (Additional file 10: Figure S2), but some isomiRs are more tissue specific than others as shown for miR-215 in the intestines (Additional file 11: Figure S3) and miR-217-5p in the pancreas (Additional file 10: Figure S2). [score:3]
IsomiRs of miR-215 in the intestine. [score:1]
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[+] score: 9
Previously, it was reported that p53, another well-known tumor suppressor, upregulates the transcription of tumor-suppressor miRNAs such as miR-34a/b/c/, miR-107, miR-145, miR-192, and miR-215, which regulate cell proliferation, apoptosis, and angiogenesis [29]. [score:9]
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[+] score: 8
Other miRNAs from this paper: hsa-mir-34a, hsa-mir-34b, hsa-mir-34c
We also examined basal expression levels of the p53 target microRNA genes: miR-34a, b, c [13, 29], and miR-215 [30, 31]], previously reported to contribute to cell cycle arrest and/or apoptotic activity of p53. [score:5]
All four microRNAs were expressed at similar (miR-34c) or higher (miR215, miR34a and b) levels in senescent cells compared to early passage cells (Figure 2B). [score:2]
We also evaluated nutlin -induced expression of four microRNA genes (miR-34a, b, c and miR-215) before and after treatment in both early passage and senescent cells. [score:1]
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[+] score: 8
Activation of tumor suppressor p53 can induce miR-194 and its clustered miR-192 and miR-215 expression [55], [57]. [score:5]
Ann Surg Oncol 57 Georges SA Biery MC Kim SY Schelter JM Guo J 2008 Coordinated regulation of cell cycle transcripts by p53-Inducible microRNAs, miR-192 and miR-215. [score:2]
miR-192 and miR-215 can induce p21Cip1 and cell cycle arrest in colon cancer cells [55]. [score:1]
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[+] score: 8
miR-192, miR-194, miR-215, miR-200c and miR-141 are downregulated and their common target ACVR2B is strongly expressed in renal childhood neoplasms. [score:8]
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[+] score: 8
The differentially expressed miR-215 has been shown to target IL17RS and IL21 [105, 106]. [score:5]
The first plot indicates the borderline significant eca-miR-215 followed by the boxplot for eca-miR-140-3p which clearly indicates that the signal for that miRNA is predominantly driven by one extreme outlier individual. [score:1]
Using DESeq2, we identified 11 miRNAs as statistically significant DEmiRs after accounting for the level of hemolysis: eca-miR-128, eca-miR-744, eca-miR-197, eca-miR-103 and the closely related eca-miR-107a, eca-miR-30d, eca-miR-140-3p, eca-miR-7, eca-miR-361-3p, eca-miR-148b-3p and eca-miR-215. [score:1]
Eight of these eleven DEmiRs were also reported by edgeR (eca-miR-7, eca-miR-148b-3p and eca-miR-215 missed the significance threshold) (Table 1). [score:1]
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[+] score: 8
For example, the up-regulation of miRNA hsa-mir-183 (1st in the prediction list), hsa-mir-215(2nd in the prediction list), hsa-mir-9 (3rd in the prediction list), hsa-mir-34a (5th in the prediction list) and down-regulation of hsa-mir-30b (4th in the prediction list) are all related to the development of lymphoma. [score:8]
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[+] score: 8
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-98, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-210, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-143, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-138-1, hsa-mir-146a, hsa-mir-193a, hsa-mir-194-1, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-302a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-369, hsa-mir-371a, hsa-mir-340, hsa-mir-335, hsa-mir-133b, hsa-mir-146b, hsa-mir-519e, hsa-mir-519c, hsa-mir-519b, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-499a, hsa-mir-504, hsa-mir-421, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-190b, hsa-mir-301b, hsa-mir-302e, hsa-mir-302f, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-320e, hsa-mir-371b, hsa-mir-499b
The action of p53 is also essential for induction of the related miRNAs miR-192, miR-194 and miR-215, which are up-regulated by genotoxic stress and are capable of inducing cell cycle arrest by causing increased expression of multiple transcripts involved in S phase and G1 and G2 checkpoints in human colon cancer samples [21] and human osteosarcoma cells [22]. [score:6]
Georges S. A. Biery M. C. Kim S. Y. Schelter J. M. Guo J. Chang A. N. Jackson A. L. Carleton M. O. Linsley P. S. Cleary M. A. Coordinated regulation of cell cycle transcripts by p53-Inducible microRNAs, miR-192 and miR-215 Cancer Res. [score:2]
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38
[+] score: 7
In GC, miR-192, miR-215, miR-25 are reported to be upregulated, whereas miR-375, miR-101 are downregulated [9– 12]. [score:7]
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[+] score: 7
Incubation of the RF24 cells with conditioned media collected from the S KOV3ip1 cells treated with miR-215, a miRNA closely associated with miR-192, did not significantly inhibit tube formation, demonstrating the unique ability of miR-192 to regulate tumour angiogenesis (Supplementary Fig. 1g). [score:4]
The cells were incubated with conditioned media collected from stable S KOV3ip1 control miRNA or miR-192 expressing cells or from ovarian or renal cancer cells treated control miRNA, miR-192, miR-194 or miR-215 mimics. [score:3]
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[+] score: 7
The five miRNAs, hsa-miR-143, hsa-miR-145, hsa-miR-200c, hsa-miR-215 and hsa-miR-34a, are regulated by TP53 and can target HNF4A and MET. [score:4]
PTEN regulates hsa-miR-21 and TP53 regulates five miRNAs, consisting of hsa-miR-143, hsa-miR-145, hsa-miR-200, hsa-miR-215 and hsa-miR-34a. [score:3]
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[+] score: 7
The miRNAs downregulated the most included the miR-141/miR-200 and miR-30 families, as well as miR-192, miR-204, and miR-215, which play key roles in maintaining epithelial cell phenotype [17, 18], and their downregulation is in accordance with the EMT-like change occurring in cultured BCD cells. [score:7]
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[+] score: 6
For instance, mir-215 and mir-301 are downregulated in colon cancer, and mir-129 is overexpressed in prostate cancer. [score:6]
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[+] score: 6
MiRNAs in group one showed higher expression in the N group but lower expression in I group, which including gga-miR-34a-5p, gga-miR-215-5p, and gga-miR-1662. [score:5]
Gga-miR-34a-5p interacted with the greatest number of immune-related genes (46), while the gga-miR-215-5p only interacted with one immune-related gene. [score:1]
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[+] score: 6
Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-20a, hsa-mir-21, hsa-mir-26a-1, hsa-mir-34a, hsa-mir-182, hsa-mir-210, hsa-mir-221, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-141, hsa-mir-144, hsa-mir-127, hsa-mir-1-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-26a-2, hsa-mir-375, hsa-mir-133b, hsa-mir-20b, hsa-mir-429, hsa-mir-451a, hsa-mir-486-1, hsa-mir-802, bta-mir-26a-2, bta-let-7f-2, bta-mir-16b, bta-mir-20a, bta-mir-21, bta-mir-221, bta-mir-34b, bta-mir-127, bta-mir-15b, bta-mir-20b, bta-mir-215, bta-mir-210, bta-let-7f-1, bta-mir-122, bta-mir-34c, bta-mir-34a, bta-mir-1-2, bta-mir-1-1, bta-mir-133a-2, bta-mir-133a-1, bta-mir-133b, bta-mir-141, bta-mir-144, bta-mir-16a, bta-mir-182, bta-mir-26a-1, bta-mir-375, bta-mir-429, bta-mir-451, bta-mir-486, bta-mir-2285a, bta-mir-2285d, bta-mir-2285b-1, bta-mir-2376, bta-mir-2285c, bta-mir-1388, bta-mir-3431, hsa-mir-451b, bta-mir-2285e-1, bta-mir-2285e-2, bta-mir-2285f-1, bta-mir-2285f-2, bta-mir-2285g-1, bta-mir-2285h, bta-mir-2285i, bta-mir-2285j-1, bta-mir-2285j-2, bta-mir-2285k-1, bta-mir-2285l, bta-mir-6119, bta-mir-2285o-1, bta-mir-2285o-2, bta-mir-2285n-1, bta-mir-2285n-2, bta-mir-2285p, bta-mir-2285m-1, bta-mir-2285m-2, bta-mir-2285n-3, bta-mir-2285n-4, bta-mir-2285o-3, bta-mir-2285o-4, bta-mir-2285m-3, bta-mir-2285m-4, bta-mir-2285o-5, bta-mir-2285m-5, bta-mir-2285n-5, bta-mir-2285n-6, bta-mir-2285n-7, bta-mir-2285k-2, bta-mir-6529a, bta-mir-2285k-3, bta-mir-2285k-4, bta-mir-2285k-5, bta-mir-2285q, bta-mir-2285r, bta-mir-2285s, bta-mir-2285t, bta-mir-2285b-2, bta-mir-2285v, hsa-mir-486-2, bta-mir-2285g-2, bta-mir-2285g-3, bta-mir-2285af-1, bta-mir-2285af-2, bta-mir-2285y, bta-mir-2285w, bta-mir-2285x, bta-mir-6529b, bta-mir-133c, bta-mir-2285z, bta-mir-2285u, bta-mir-2285aa, bta-mir-2285ab, bta-mir-2285ac, bta-mir-2285ad, bta-mir-2285ae, bta-mir-2285ag, bta-mir-2285ah, bta-mir-2285ai, bta-mir-2285aj, bta-mir-2285ak, bta-mir-2285al, bta-mir-2285am, bta-mir-2285ar, bta-mir-2285as-1, bta-mir-2285as-2, bta-mir-2285as-3, bta-mir-2285at-1, bta-mir-2285at-2, bta-mir-2285at-3, bta-mir-2285at-4, bta-mir-2285au, bta-mir-2285av, bta-mir-2285aw, bta-mir-2285ax-1, bta-mir-2285ax-2, bta-mir-2285ax-3, bta-mir-2285ay, bta-mir-2285az, bta-mir-2285an, bta-mir-2285ao-1, bta-mir-2285ao-2, bta-mir-2285ap, bta-mir-2285ao-3, bta-mir-2285aq-1, bta-mir-2285aq-2, bta-mir-2285ba-1, bta-mir-2285ba-2, bta-mir-2285bb, bta-mir-2285bc, bta-mir-2285bd, bta-mir-2285be, bta-mir-2285bf-1, bta-mir-2285bf-2, bta-mir-2285bf-3, bta-mir-2285bg, bta-mir-2285bh, bta-mir-2285bi-1, bta-mir-2285bi-2, bta-mir-2285bj-1, bta-mir-2285bj-2, bta-mir-2285bk, bta-mir-2285bl, bta-mir-2285bm, bta-mir-2285bn, bta-mir-2285bo, bta-mir-2285bp, bta-mir-2285bq, bta-mir-2285br, bta-mir-2285bs, bta-mir-2285bt, bta-mir-2285bu-1, bta-mir-2285bu-2, bta-mir-2285bv, bta-mir-2285bw, bta-mir-2285bx, bta-mir-2285by, bta-mir-2285bz, bta-mir-2285ca, bta-mir-2285cb, bta-mir-2285cc, bta-mir-2285cd, bta-mir-2285ce, bta-mir-2285cf, bta-mir-2285cg, bta-mir-2285ch, bta-mir-2285ci, bta-mir-2285cj, bta-mir-2285ck, bta-mir-2285cl, bta-mir-2285cm, bta-mir-2285cn, bta-mir-2285co, bta-mir-2285cp, bta-mir-2285cq, bta-mir-2285cr-1, bta-mir-2285cr-2, bta-mir-2285cs, bta-mir-2285ct, bta-mir-2285cu, bta-mir-2285cv-1, bta-mir-2285cv-2, bta-mir-2285cw-1, bta-mir-2285cw-2, bta-mir-2285cx, bta-mir-2285cy, bta-mir-2285cz, bta-mir-2285da, bta-mir-2285db, bta-mir-2285dc, bta-mir-2285dd, bta-mir-2285de, bta-mir-2285df, bta-mir-2285dg, bta-mir-2285dh, bta-mir-2285di, bta-mir-2285dj, bta-mir-2285dk, bta-mir-2285dl-1, bta-mir-2285dl-2, bta-mir-2285dm, hsa-mir-6529
Accordingly, the three miRNAs (Fig.   5a) were expressed predominantly in liver (miR-122, 88-fold higher than in any other tissue), muscle/heart (miR-133, 254-fold higher) and intestine (miR-215, 150-fold higher). [score:3]
We first profiled three miRNAs, miR-122, miR-133a and miR-215, known to be tissue-specific in humans [37, 38]. [score:1]
Among miRNAs found to be enriched in plasma, we confirmed miR-122 (liver), miR-133a (muscle) and miR-215 (intestine) to be tissue-enriched, as reported for other species. [score:1]
We then sought to validate the results for these eight miRNAs (miR-122, miR-215, miR-133a, miR-144, miR-451, and miR-6119-5p, miR-26a and let-7f) using samples from an independent group of animals (four Holstein-Friesian cross cows, aged between 24 and 48 months, in late pregnancy or post-partum) and we confirmed differences in plasma and cell levels of seven miRNAs (Additional file  2); levels of miR-133a were very low (Ct 34–37) in the original group of animals and were undetectable in this second group. [score:1]
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Since, among these differentially expressed miRNAs, miR-183, miR-215, and miR-363 were found downregulated in both the ectopic and eutopic tissues, the authors selected miR-183 for validation of further functional studies. [score:6]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-134, mmu-mir-137, mmu-mir-138-2, mmu-mir-145a, mmu-mir-24-1, hsa-mir-192, mmu-mir-194-1, mmu-mir-200b, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-221, hsa-mir-200b, mmu-mir-296, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-134, hsa-mir-138-1, hsa-mir-194-1, mmu-mir-192, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-24-2, mmu-mir-346, hsa-mir-200c, mmu-mir-17, mmu-mir-25, mmu-mir-200c, mmu-mir-221, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-200a, hsa-mir-296, hsa-mir-369, hsa-mir-346, mmu-mir-215, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-221, gga-mir-17, gga-mir-138-1, gga-mir-124a, gga-mir-194, gga-mir-215, gga-mir-137, gga-mir-7-2, gga-mir-138-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-200a, gga-mir-200b, gga-mir-124b, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-7-3, gga-mir-7-1, gga-mir-24, gga-mir-7b, gga-mir-9-2, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-192, dre-mir-221, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-17a-1, dre-mir-17a-2, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-25, dre-mir-92b, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-145, dre-mir-194a, dre-mir-194b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, mmu-mir-470, hsa-mir-485, hsa-mir-496, dre-let-7j, mmu-mir-485, mmu-mir-543, mmu-mir-369, hsa-mir-92b, gga-mir-9-1, hsa-mir-671, mmu-mir-671, mmu-mir-496a, mmu-mir-92b, hsa-mir-543, gga-mir-124a-2, mmu-mir-145b, mmu-let-7j, mmu-mir-496b, mmu-let-7k, gga-mir-124c, gga-mir-9-3, gga-mir-145, dre-mir-138-2, dre-mir-24b, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-let-7l-1, gga-let-7l-2, gga-mir-9b-2
Mdm2 is negatively regulated by several miRNAs including miR-192 (Pichiorri et al., 2010), miR-194 (Pichiorri et al., 2010), miR-215 (Pichiorri et al., 2010), miR-221 (Kim et al., 2010), and miR-17 (Li and Yang, 2012) in different cellular contexts; however, whether these or other miRNAs regulate Mdm2 expression during the CNS development must be determined. [score:6]
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BCL6 modulates the B cell response inducing tolerance to DNA damage -induced apoptosis by suppressing TP53 in GC B cells, [48]; while P53 controls the cell cycle at two distinctive checkpoints (G1/S and G2/M) by the regulation of miR-107, miR-145, miR-34, and of the miRNA clusters miR-15a/miR-16 and miR-192/miR-194/miR-215, able to target many cell cycle-related genes [49]. [score:6]
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Van Jaarsveld et al. compared the miR expression profiles of cisplatin-sensitive and -resistant ovarian cancer cells, revealing that high expression of miR-141, miR-200c, miR-215, and miR-421 and low expression of miR-492-5p correlated with increased cisplatin resistance [61]. [score:6]
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Finally, we performed a miRNA target enrichment analysis of the list of switch genes by using miRTarBase [62] and we found miR-335 and miR-215 as the most enriched miRNAs with the highest number of targets among switch genes (Supplementary Table  S11). [score:5]
Interestingly, miR-335 is capable of inducing glioma cell differentiation by activating cAMP/protein kinase A (PKA) pathway [83], while the induction of miR-215 serves for maintaining glioblastoma stem-like cells [84]. [score:1]
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For example, Pichiorri et al. [83] identified that in multiple myeloma, three miRNAs (miR-192, miR-194 and miR-215) are transcriptionally activated by p53 to suppress Mdm2 expression via directly binding to its mRNA, thereby protecting p53 from degradation. [score:6]
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Kim et al. [64] found that p53 up-regulated miR-200 and miR-192 family members and described the role of p53 in regulating epithelial-mesenchymal transition (EMT) in HCC through the induction of specific effector microRNAs including miR-141, miR-192, miR-194, miR-200b, miR-200c, and miR-215. [score:5]
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Moreover, miR-215 inhibits activated leukocyte cell adhesion molecule (ALCAM) expression at the posttranscriptional level and can increase the migration of gastric cancer cells (Ref. [score:5]
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For example, the common target ACVR2B of five miRNAs (miRNA-192, miRNA-194, miRNA-215, miRNA-200c and miRNA-141) is strongly expressed in renal childhood neoplasms [57]. [score:5]
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Up-regulated miRNAs in NSCLC included miR-142-5p, miR-148b, miR-148a, miR-369-3p, miR-215, miR-152 and miR-155, whereas down-regulated miRNAs were miR-373 and miR-138-I. Some of these miRNAs have a well-characterized association with cancer progression, e. g., miR-10b, miR-21, miR-30a, miR-30e, miR-125b, miR-141, miR-200b, miR-200c, and miR-205 [90]. [score:5]
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As illustrated in Fig 3, 7 miRNAs including miR-29c, miR-217, miR-375, miR-215, miR-19b, miR-133a and let-7a had relatively low and stable expression levels (P < 0.05) in early period, and increased significantly (P < 0.01) from 12 to 13 weeks when the gonads entered into rapid development. [score:4]
According to previous reports and our sequencing results, 9 miRNAs, including miR-29c-3p, miR-375, miR-215-5p, miR-9-5p, miR-19b-3p, miR-133a-3p, let-7a, miR-217-5p and miR-155 were determined as candidates. [score:1]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-101-1, hsa-mir-106a, hsa-mir-107, hsa-mir-16-2, hsa-mir-192, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-129-1, hsa-mir-148a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-210, hsa-mir-212, hsa-mir-214, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-129-2, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-130b, hsa-mir-376c, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-20b, hsa-mir-429, hsa-mir-449a, hsa-mir-433, hsa-mir-451a, hsa-mir-193b, hsa-mir-520d, hsa-mir-503, hsa-mir-92b, hsa-mir-610, hsa-mir-630, hsa-mir-650, hsa-mir-449b, hsa-mir-421, hsa-mir-449c, hsa-mir-378d-2, hsa-mir-744, hsa-mir-1207, hsa-mir-1266, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-4512, hsa-mir-378i, hsa-mir-203b, hsa-mir-451b, hsa-mir-378j
Moreover, GC patients with over -expression of miR-107 [28, 29, 30], miR-143 [40], miR-145 [41, 42], miR-181b/c [17, 47, 48, 55, 56], miR-196a/b [59], miR-20b [23, 66], miR-23a/b [77, 78, 79], miR-34 [17, 47, 48, 55, 56] and miR-630 [100] and decreased expression of miR-1 [111], miR-1207-5p [121], miR-125a-3p/-5p [24, 125, 126, 127], miR-185 [140], miR-193b [60], miR-20a [111], miR-206 [150, 151], miR-215 [142], miR-217 [153], miR-27a [111], miR-29c [169], miR-34a [172, 173], miR-423-5p [111], and miR-520d-3p [99] indicate advanced tumor stage or TNM stage. [score:5]
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57
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181a-1, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-mir-15b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-141, hsa-mir-143, hsa-mir-152, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-184, hsa-mir-200c, hsa-mir-155, hsa-mir-29c, hsa-mir-200a, hsa-mir-99b, hsa-mir-296, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-342, hsa-mir-148b, hsa-mir-451a, ssc-mir-125b-2, ssc-mir-148a, ssc-mir-15b, ssc-mir-184, ssc-mir-224, ssc-mir-23a, ssc-mir-24-1, ssc-mir-26a, ssc-mir-29b-1, ssc-let-7f-1, ssc-mir-103-1, ssc-mir-21, ssc-mir-29c, hsa-mir-486-1, hsa-mir-499a, hsa-mir-671, hsa-mir-378d-2, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-16b, bta-mir-21, bta-mir-499, bta-mir-99a, bta-mir-125b-1, bta-mir-126, bta-mir-181a-2, bta-mir-27b, bta-mir-31, bta-mir-15b, bta-mir-215, bta-mir-30e, bta-mir-148b, bta-mir-192, bta-mir-200a, bta-mir-200c, bta-mir-23a, bta-mir-29b-2, bta-mir-29c, bta-mir-10b, bta-mir-24-2, bta-mir-30a, bta-mir-200b, bta-let-7a-1, bta-mir-342, bta-let-7f-1, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-125b-2, bta-mir-15a, bta-mir-99b, hsa-mir-664a, ssc-mir-99b, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, bta-mir-141, bta-mir-143, bta-mir-146a, bta-mir-152, bta-mir-155, bta-mir-16a, bta-mir-184, bta-mir-24-1, bta-mir-223, bta-mir-224, bta-mir-26a-1, bta-mir-296, bta-mir-29d, bta-mir-378-1, bta-mir-451, bta-mir-486, bta-mir-671, bta-mir-29e, bta-mir-29b-1, bta-mir-181a-1, ssc-mir-181a-1, ssc-mir-215, ssc-mir-30a, bta-mir-2318, bta-mir-2339, bta-mir-2430, bta-mir-664a, bta-mir-378-2, ssc-let-7a-1, ssc-mir-378-1, ssc-mir-29a, ssc-mir-30e, ssc-mir-499, ssc-mir-143, ssc-mir-10b, ssc-mir-486-1, ssc-mir-152, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-99a, ssc-mir-148b, ssc-mir-664, ssc-mir-192, ssc-mir-342, ssc-mir-125b-1, oar-mir-21, oar-mir-29a, oar-mir-125b, oar-mir-181a-1, hsa-mir-378b, hsa-mir-378c, ssc-mir-296, ssc-mir-155, ssc-mir-146a, bta-mir-148c, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-486-2, hsa-mir-664b, hsa-mir-378j, ssc-let-7f-2, ssc-mir-29b-2, ssc-mir-31, ssc-mir-671, bta-mir-378b, bta-mir-378c, hsa-mir-486-2, oar-let-7a, oar-let-7f, oar-mir-103, oar-mir-10b, oar-mir-143, oar-mir-148a, oar-mir-152, oar-mir-16b, oar-mir-181a-2, oar-mir-200a, oar-mir-200b, oar-mir-200c, oar-mir-23a, oar-mir-26a, oar-mir-29b-1, oar-mir-30a, oar-mir-99a, bta-mir-664b, chi-let-7a, chi-let-7f, chi-mir-103, chi-mir-10b, chi-mir-125b, chi-mir-126, chi-mir-141, chi-mir-143, chi-mir-146a, chi-mir-148a, chi-mir-148b, chi-mir-155, chi-mir-15a, chi-mir-15b, chi-mir-16a, chi-mir-16b, chi-mir-184, chi-mir-192, chi-mir-200a, chi-mir-200b, chi-mir-200c, chi-mir-215, chi-mir-21, chi-mir-223, chi-mir-224, chi-mir-2318, chi-mir-23a, chi-mir-24, chi-mir-26a, chi-mir-27b, chi-mir-296, chi-mir-29a, chi-mir-29b, chi-mir-29c, chi-mir-30a, chi-mir-30e, chi-mir-342, chi-mir-378, chi-mir-451, chi-mir-499, chi-mir-671, chi-mir-99a, chi-mir-99b, bta-mir-378d, ssc-mir-378b, oar-mir-29b-2, ssc-mir-141, ssc-mir-200b, ssc-mir-223, bta-mir-148d
Ye et al. (2012) examined miRNA expression in the duodenum of E. coli F18-sensitive and -resistant weaned piglets and identified 12 candidate miRNA (ssc-miR-143, ssc-let-7f, ssc-miR-30e, ssc-miR-148a, ssc-miR-148b, ssc-miR-181a, ssc-miR-192, ssc-miR-27b, ssc-miR-15b, ssc-miR-21, ssc-miR-215, and ssc-miR-152) disease markers. [score:5]
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58
[+] score: 5
Moreover, miR-192 is reported to suppress metastasis of CRC [46] and its synthesis, along with that of miR-215 (also highly represented in our 254 miRNA dataset), is induced by p53 and shown to play an important regulatory role of genes involved in the TGF-β signalling pathway [47], [48]. [score:4]
This analysis revealed the prominence in all three EVs of members from the following families: let-7 (12/12 members observed, let-7a/b/c/d/e/f/g/i, miR-98-5p), miR-181 (6/6, miR-181a-1/a-2/b-1/b-2/c/d), miR-30 (6/6, miR-30a/b/c-1/c-2/d/e), miR-320 (7/8, miR-320a/b-1/b-2/c-1/c-2/d-1/d-2), miR-8 (5/5, miR-141, miR-200a/b/c and miR-429), miR-17 (6/8, miR-106a/b, miR-17, miR-18a, miR-20a and miR-93), miR-192 (2/2, miR-192 and miR-215) and miR-25 (3/4, mir-25 and mir-92a/b). [score:1]
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59
[+] score: 5
Ectopic expression of miR-192 and miR-215 increased E-cadherin levels by targeting ZEB2 [31]. [score:5]
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60
[+] score: 4
MiR-342-5p, miR-3058-3p, let-7f-5p, miR-1961, miR-301b-3p, miR-98-5p, miR-1251-5p, miR-215-5p, miR-881-5p, miR-135a-2-3p, and miR-33-3p may regulate the expression of insulin-like growth factor 1 (IGF1) or insulin-like growth factor 2 (IGF2), two molecules that could rescue behavior and memory deficits via lowering A β levels [28, 29]. [score:4]
[1 to 20 of 1 sentences]
61
[+] score: 4
Although many IBD -associated miRNAs did not appear to be dysregulated in preterm NEC tissues, several miRNAs, including miR-223, miR-132, miR-146b-3p, miR-215, miR-375, miR-31 and miR-141, were regulated in both IBD and NEC. [score:3]
Levels of 15 miRNAs: miR-223, miR-1290, miR-4725-3p, miR-4793-3p, miR-410, miR-187, miR-375, miR-203, miR-200b-5p, miR-194-3p, miR-200a, miR-215, miR-31, miR-192-3p and miR-141 were significantly different between NEC and SIP tissues (0.12–59.05 fold; Table 2). [score:1]
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62
[+] score: 4
Other miRNAs from this paper: hsa-mir-21, hsa-mir-144, hsa-mir-30e
Recently we identified changes in expression in peripheral blood of four microRNAs (miR-21, miR-30e, miR-215 and miR-144) in response to DE exposure in the same subjects that were involved in this study [19]. [score:3]
A total of 7 probes overlapping with microRNAs miR-21, miR-30e, miR-215 and miR-144 were also identified and used in subsequent analysis. [score:1]
[1 to 20 of 2 sentences]
63
[+] score: 4
However, miR-215 [31], miR-375 [32], miR-141, and miR-200c [33], miR-200a [34], miR-429 [35], miR-625 [36], and miR-18a [37] have already been shown to be inversely correlated with the EMT, and they were found downregulated in this subtype. [score:4]
[1 to 20 of 1 sentences]
64
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-25, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-198, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-216a, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-142, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-186, hsa-mir-188, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-362, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-382, hsa-mir-340, hsa-mir-328, hsa-mir-342, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-339, hsa-mir-335, hsa-mir-345, hsa-mir-196b, hsa-mir-424, hsa-mir-425, hsa-mir-20b, hsa-mir-451a, hsa-mir-409, hsa-mir-484, hsa-mir-486-1, hsa-mir-487a, hsa-mir-511, hsa-mir-146b, hsa-mir-496, hsa-mir-181d, hsa-mir-523, hsa-mir-518d, hsa-mir-499a, hsa-mir-501, hsa-mir-532, hsa-mir-487b, hsa-mir-551a, hsa-mir-92b, hsa-mir-572, hsa-mir-580, hsa-mir-550a-1, hsa-mir-550a-2, hsa-mir-590, hsa-mir-599, hsa-mir-612, hsa-mir-624, hsa-mir-625, hsa-mir-627, hsa-mir-629, hsa-mir-33b, hsa-mir-633, hsa-mir-638, hsa-mir-644a, hsa-mir-650, hsa-mir-548d-1, hsa-mir-449b, hsa-mir-550a-3, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-454, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-708, hsa-mir-216b, hsa-mir-1290, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-3151, hsa-mir-320e, hsa-mir-378c, hsa-mir-550b-1, hsa-mir-550b-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-219b, hsa-mir-203b, hsa-mir-451b, hsa-mir-499b, hsa-mir-378j, hsa-mir-486-2
In contrast, deregulation of the expression of miR-9, miR-33, miR-92a, miR-142-3p, miR-146a, miR-181a/c, miR-210, miR-215, miR-369-5p, miR-335, miR-454, miR-496, miR-518d, and miR-599 was associated with an unfavorable long-term clinical outcome in ALL patients [65, 67– 73]. [score:4]
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65
[+] score: 4
MiR-215-5p (FC 3.1; p value 0.02) and miR-1285 (FC 2.9; p value 7.35x10 [-5]) were the most upregulated miRNAs. [score:4]
[1 to 20 of 1 sentences]
66
[+] score: 4
Figure 6D gives an example of miR-215, in which a 5′isomiR (UGACCU) is expressed as the dominant transcript by far in liver and kidneys. [score:3]
The miR-215 canoncial sequence (miRBase, (30)) is assigned a value of 1 for each tissue type and the isomiR value equals the total number of isomiR sequence reads/total number of canonical sequencing reads for each tissue. [score:1]
[1 to 20 of 2 sentences]
67
[+] score: 4
Among the up-regulated miRNAs identified in chemoresistant OS samples in this study, miR-140, miR-215 and miR-221 have been reported to induce human OS chemoresistance [20- 22]. [score:4]
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68
[+] score: 4
for c) miR-106b-3p and d) miR-215 are shown by disease groups and NYHA classes, respectively. [score:3]
Eight miRNAs (miR-215, miR-30d-5p, miR-218–5p, miR-146–5p, miR-21–5p, miR-30e-3p, miR-23a-3p and miR-181a-5p) were found to be differentially detected between the NYHA classes (ANOVA, p<0.05), but they failed to pass Benjamini-Hochberg correction for false positivity in multiple testing (Figs. 3B and 3D). [score:1]
[1 to 20 of 2 sentences]
69
[+] score: 4
Similarly, miR-215 induced chemoresistance to MTX in U2OS cells. [score:1]
Braun et al. found that miRNAs such as miR-192 and miR-215 are p53 responsive miRNAs that are capable of causing cell cycle arrest in the osteosarcoma cell line U2OS that carries a wild-type p53 (Braun et al., 2008). [score:1]
Some of the first known miRNAs that have been associated with drug sensitivity are miR-140 and miR-215 (Song et al., 2009, 2010; Zhu et al., 2012). [score:1]
Molecular mechanism of chemoresistance by miR-215 in osteosarcoma and colon cancer cells. [score:1]
[1 to 20 of 4 sentences]
70
[+] score: 4
For example, miR-215, miR-200c, miR-192, miR-194 and miR-141 were downregulated in Kidney Neoplasms [92]. [score:4]
[1 to 20 of 1 sentences]
71
[+] score: 4
MiR-30c, miR-192 and miR-215 did not show correlation between the results of the reporter gene assay and the expression levels observed in sALS that could explain the suppression of NFL mRNA observed in sALS SC (data not shown). [score:4]
[1 to 20 of 1 sentences]
72
[+] score: 4
The same group recently reported that miR-215 conferred chemoresistance to methotrexate in osteosarcoma cells in vitro by suppression of a cell cycle-regulated nuclear and centrosome protein [12]. [score:4]
[1 to 20 of 1 sentences]
73
[+] score: 4
Other miRNAs from this paper: hsa-mir-200b, hsa-mir-200c, hsa-mir-200a, hsa-mir-503
Liu F. You X. Chi X. Wang T. Ye L. Niu J. Zhang X. Hepatitis B virus X protein mutant HBxΔ127 promotes proliferation of hepatoma cells through up -regulating miR-215 targeting PTPRTBiochem. [score:4]
[1 to 20 of 1 sentences]
74
[+] score: 4
Our data and the direction of overlapping transcripts suggest that miR-215 may have been annotated to the wrong genomic strand. [score:2]
The method used to predict miR-215 successfully predicted 81 out of 109 known miRNAs from a reference set, but around 20% (17/81) were predicted on the wrong strand of the genome [33]. [score:1]
One of the edited antisense pri-miRNA sequences is derived from the DNA strand opposite the computationally predicted miR-215 [33]. [score:1]
[1 to 20 of 3 sentences]
75
[+] score: 3
Jin et al. reported that both miR-192 and miR-215 were over-expressed in vivo and exerted cell growth and migration-promoting effects in vitro [44]. [score:3]
[1 to 20 of 1 sentences]
76
[+] score: 3
A neighboring group of miRNAs (miR-192, miR-194, and miR-215) shared similar expression patterns but particularly in the gastrointestinal organs (r = 0.912, Figure 2). [score:3]
[1 to 20 of 1 sentences]
77
[+] score: 3
Emerging evidence has demonstrated that WT p53 can also indirectly silence EMT-inducing transcription factors though the transcriptional regulation of some miRNAs, such as miR-34, miR-130b, miR-145, miR-192, miR-215 and miR-200c [21, 22, 23, 24, 25, 26, 27]. [score:3]
[1 to 20 of 1 sentences]
78
[+] score: 3
Specifically, Wijnhoven et al. [10] have shown that miR-203 and miR-205 are high in normal squamous epithelium and low in columnar epithelia, while miR-21, miR-143, miR-145, miR-194, and miR-215 are significantly upregulated in columnar tissues compared with normal squamous epithelium. [score:3]
[1 to 20 of 1 sentences]
79
[+] score: 3
In gastric cancer, RUNX1 could reduce the aggressive function of miR-215, thus acting as a tumor suppressor [30]. [score:3]
[1 to 20 of 1 sentences]
80
[+] score: 3
Eleven microRNAs that were differentially expressed and common in 2 of the 4 cell types were found to be miR-17, miR-21, miR-29c, miR-141, miR-142-3p, miR-215, miR-494, miRPlus-E1072, miRPlus-E1192, miR-1248, and miR-1973 (Fig. 5). [score:3]
[1 to 20 of 1 sentences]
81
[+] score: 3
Of 262 miRNAs in the network significantly correlated with at least one pathway, 8020 miRNA pairs (out of >20,000 possible pairs) were candidates for pathway cotargeting, including hsa-miR-497 and hsa-miR-503 (ER, Ras, and TGF-β), hsa-miR-20a and hsa-miR-372 (EGFR and p53), and hsa-miR-192 and hsa-miR-215 (BRCA1 and HER2). [score:3]
[1 to 20 of 1 sentences]
82
[+] score: 3
Members of the miR-888 cluster and miR-215 are differentially expressed in the epididymis. [score:3]
[1 to 20 of 1 sentences]
83
[+] score: 3
MiR-192 and miR-215 are intestine-specific miRNAs and miR-122 is a liver-specific miRNA. [score:1]
As shown in Fig. 1B, intestine-specific miR-192 and miR-215 levels and hepatic miR-122 levels in the immunoprecipitated samples were approximately 10-fold and 3-fold higher, respectively, and also significantly lower than those in total plasma exosomes. [score:1]
Intestine-specific miR-192 and miR-215 levels in immunoprecipitated exosomes were significantly higher (approximately 10- and 3-fold, respectively) than those in total plasma exosomes (P < 0.05, Fig. 1B). [score:1]
[1 to 20 of 3 sentences]
84
[+] score: 3
The MC phenotypic transition is crucial for DN progression, and miR-215 has been shown to function as a key endogenous gene-silencing factor that mediates the TGF-β1 -induced MC activation and fibronectin expression via the CTNNBIP1/β-catenin pathway [27]. [score:3]
[1 to 20 of 1 sentences]
85
[+] score: 2
Finally in pigs ssc-mir-215-5p has been reported to be present in the head and organs of 33 day old embryos. [score:1]
These were gga-mir-control, as an endogenous positive control and for calculating relative expression; gga-mir-183, which was not present in either fluid, as an endogenous negative control; gga-mir-2188, gga-mir-30c-5p, gga-mir-215-5p and gga-mir-92-3p all of which were present in both fluids. [score:1]
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86
[+] score: 2
For example, the supervised classifier was not able to identify the miRNA-gene relations in “Hence, miR-192 and miR-215 can act as effectors as well as regulators of p53” (PMID 19074875), while IBRel identified both relations. [score:2]
[1 to 20 of 1 sentences]
87
[+] score: 2
Many miRNAs were reported to be associated with GC development in the past decade, including miR-146a (Yao et al., 2013), miR-204-5p (Zhang et al., 2015), miR-486 (Oh et al., 2011), miR-192 (Jin et al., 2011), miR-215 (Jin et al., 2011), miR-34b/c (Suzuki et al., 2010), miR-29a (Cui et al., 2011), miR-409-3p (Li et al., 2012a), and miR-296-5p (Li et al., 2014). [score:2]
[1 to 20 of 1 sentences]
88
[+] score: 2
de Krijger et al stated that microRNAs such as miR-21, miR-34a, miR-143, miR-192, miR-215, and miR-221 were involved in CRC metastasis (25). [score:1]
As shown in Fig. 3B, miR-21, miR-192, miR-221, and U6 snRNA were detected from the exosomes of the three CRC cell lines, especially miR-21 was strongly detected from the exosomes of SW480 and WiDr cells; miR-34a was weakly detected from the exosomes of WiDr; miR-215 was weakly detected from the exosomes of HCT-15; and miR-143 was not detected from the exosomes of the three CRC cell lines. [score:1]
[1 to 20 of 2 sentences]
89
[+] score: 2
Like miR-71, some miRNAs had particularly high copies in C. sinensis, including miR-277b, miR-71c and miR-215. [score:1]
When the copy numbers were higher than 100,000, only 4 kinds of miRNA were represented (miR-71, miR-277b, miR-71c and miR-215). [score:1]
[1 to 20 of 2 sentences]
90
[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-139, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-210, hsa-mir-181a-1, hsa-mir-214, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-190a, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-370, hsa-mir-373, hsa-mir-374a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-429, hsa-mir-491, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, hsa-mir-517a, hsa-mir-500a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-637, hsa-mir-151b, hsa-mir-298, hsa-mir-190b, hsa-mir-374b, hsa-mir-500b, hsa-mir-374c, hsa-mir-219b, hsa-mir-203b
Coordinated regulation of cell cycle transcripts by p53-Inducible microRNAs, miR-192 and miR-215. [score:2]
[1 to 20 of 1 sentences]
91
[+] score: 1
From the prediction, the experimental data from cow milk study validated 9 transportable milk miRNAs in human blood, including bta-miR-487b, miR-181b, miR-421, miR-215, let-7c, miR-301a, miR-432, miR-127, and miR-184. [score:1]
[1 to 20 of 1 sentences]
92
[+] score: 1
miR-192 and miR-215 share identical seed sequences, and only differ by two nucleotides [10]. [score:1]
[1 to 20 of 1 sentences]
93
[+] score: 1
, miR-194, miR-207, miR-107 [13], miR-215, miR-192 14, 15 miR-16-1, miR-143, miR-145, and miR-216 [9]. [score:1]
[1 to 20 of 1 sentences]
94
[+] score: 1
Among the conserved family of miRs identified by this approach, miR-71 was having the highest number of reads followed by mir-277 and miR-215, suggesting their role in parasite’s survival and metabolism inside the host. [score:1]
[1 to 20 of 1 sentences]
95
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-99a, hsa-mir-100, hsa-mir-101-1, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-10a, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-141, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-194-1, hsa-mir-195, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-130b, hsa-mir-302c, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-324, hsa-mir-451a, hsa-mir-483, hsa-mir-484, hsa-mir-486-1, hsa-mir-500a, hsa-mir-92b, hsa-mir-595, hsa-mir-596, hsa-mir-421, hsa-mir-378d-2, hsa-mir-744, hsa-mir-885, hsa-mir-939, hsa-mir-940, hsa-mir-1229, hsa-mir-1233-1, hsa-mir-1290, hsa-mir-1246, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, hsa-mir-378b, hsa-mir-378c, hsa-mir-4306, hsa-mir-4286, hsa-mir-500b, hsa-mir-1233-2, hsa-mir-3935, hsa-mir-642b, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-3976, hsa-mir-4644, hsa-mir-203b, hsa-mir-451b, hsa-mir-378j, hsa-mir-486-2
Similarly, other groups have identified several circulating miRNAs as non-invasive diagnostic biomarkers, such as miR-21, miR-122, miR-223, miR-15b, miR-130b, miR-101, miR-483, miR-125, miR-143, miR-215, miR-200, miR-939, and miR-595 [44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56]. [score:1]
[1 to 20 of 1 sentences]
96
[+] score: 1
However, some miRNAs own oncogenic property, such as miR-125, miR-9, miR-30, miR-21, and miR-215 [125, 126]. [score:1]
[1 to 20 of 1 sentences]
97
[+] score: 1
Recent studies have demonstrated that miRs might influence the progression of osteosarcoma via pathways involving CD44, such as miR-140 and miR-215 32 33. [score:1]
[1 to 20 of 1 sentences]
98
[+] score: 1
Other miRNAs from this paper: hsa-mir-27a, hsa-mir-140, hsa-mir-144, hsa-mir-193b
Karaayvaz M Pal T Song B Zhang C Georgakopoulos P Mehmood S Burke S Shroyer K Ju J Prognostic significance of miR-215 in colon cancerClin Colorectal Cancer. [score:1]
[1 to 20 of 1 sentences]
99
[+] score: 1
Of these, nine (gga-mir-1b, gga-mir-7, gga-mir-7b, gga-mir-10b, gga-mir-31, gga-mir-130b, gga-mir-204, gga-mir-215, gga-mir-489) are increased, and five (gga-mir-223, gga-mir-124b, gga-mir-140, gga-mir-183, gga-mir-222a) are decreased in CD30 [hi] cells. [score:1]
[1 to 20 of 1 sentences]
100
[+] score: 1
As for CRC, previous study revealed that combined the other five miRNAs (miR-21–5p, miR-103a-3p, miR-106b-5p, miR-143–5p, and miR-215), their prognostic and predictive role in predicting which patients benefit from adjuvant chemotherapy for stage II colon cancer [25], while the role of miR-20a-5p have not been explored in CRC yet. [score:1]
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