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53 publications mentioning hsa-mir-216a

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-216a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 283
Other miRNAs from this paper: mmu-mir-216a, mmu-mir-216b, hsa-mir-216b, mmu-mir-216c
Our data showed that JAK2 expression was obviously downregulated by miR-216a overexpression in both MGC-803 and BGC-823 cells (P<0.05, respectively, Figure 5B and 5C). [score:8]
Notably, miR-216a overexpression reduced the expression of phosphorylated STAT3 and its downstream targets including Slug, Snail and Twist in MGC-803 cells (P<0.05, respectively, Figure 6). [score:7]
Previous study reports that miR-216a expression is upregulated by by the androgen pathway in a ligand -dependent manner in HCC [18]. [score:6]
org/10.3390/ijms17060945 10 Zhang J Xu K Shi L Zhang L Zhao Z Xu H Liang F Li H Zhao Y Xu X Tian Y Overexpression of MicroRNA-216a suppresses proliferation, migration, and invasion of glioma cells by targeting leucine-rich repeat-containing G protein-coupled receptor 5Oncol Res 2017 https://doi. [score:6]
miR-216a expression is downregulated in GC tissues and cells. [score:6]
miR-216a inhibits migration, invasion and EMT process of GC cells probably by inhibiting activation of JAK2/STAT3 pathway. [score:5]
miR-216a inhibited migration, invasion and EMT process of GC cells probably by targeting JAK2/STAT3 pathway. [score:5]
miR-216a suppresses invasion, migration and proliferation of glioma cells by inhibiting leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5)[10]. [score:5]
miR-216a inhibits migration and invasion of GC cells probably by targeting JAK2/STAT3 pathway. [score:5]
Our results demonstrated miR-216a inversely modulated activation of JAK2/STAT3 pathway and the expressions of its downstream targets including Slug, Snail and Twist in GC cells. [score:5]
Thus, predicting and confirming the targets of miR-216a are important to disclose the molecular mechanisms by which miR-216a suppressed metastasis of GC. [score:5]
Figure 8 (A) SGC-7901 cells that were transfected with miR-216a inhibitors (anti-miR-216a) were treated with the JAK2 inhibitor SAR317461 and DMSO, respectively. [score:5]
JAK2 mRNA and protein expression levels were determined after miR-216a overexpression. [score:5]
Interestingly, miR-216a overexpression led to increased expression E-cadherin and decreased levels of N-cadherin and Vimentin in MGC-803 cells (P<0.05, respectively, Figure 4A). [score:5]
Thus, we hypothesized that miR-216a inhibited EMT process and metastasis of GC cells probably by targeting JAK2/STAT3 pathway. [score:5]
Potential targets of miR-216a were predicted using the public database TargetScan (http://www. [score:5]
In turn, miR-216a knockdown facilitated EMT process of SGC-7901 cells with decreased E-cadherin and increased N-cadherin and Vimentin expression, as determined by immunoblotting and IF results (P<0.05, respectively, Figure 4C and 4D). [score:4]
miR-216a directly targets JAK2 in GC cells. [score:4]
The JAK2 inhibitor SAR317461 reverses the effects of miR-216a knockdown in GC cells. [score:4]
JAK2 is a direct target of miR-216a in GC cells. [score:4]
Furthermore, the JAK2 inhibitor SAR317461 was used for inactivation of JAK2/STAT3 pathway in miR-216a down -regulating GC cells. [score:4]
SAR317461 treatment blocked JAK2/STAT3 pathway and suppressed migration, invasion and EMT process of SGC-7901 cells with miR-216a knockdown (P<0.05, respectively, Figure 8A-8C). [score:4]
On the other hand, miR-216a was knocked down by miR-216a inhibitors in SGC-7901 cells (P<0.05, Figure 2D). [score:4]
Based on these findings, we suggest that JAK2 is a potential direct target of miR-216a in GC cells. [score:4]
miR-216a was found to be downregulated in GC tissues than in matched non-tumor tissues (P<0.05, Figure 1A). [score:4]
miR-216a underexpression associates with malignant clinical features and poor prognosis of GC patients. [score:3]
The mechanisms underlying the aberrant expression of miR-216a in human cancer is largely unknown. [score:3]
JAK2/STAT3 functions in miR-216a inhibited EMT process and metastasis of GC cells. [score:3]
miR-216a has recently been reported to play a tumor suppressive role in human cancer including glioma [10], colorectal cancer (CRC)[11] and pancreatic cancer [12, 13]. [score:3]
IF results further confirmed the changes of E-cadherin and Vimentin expression after miR-216a restoration (Figure 4B). [score:3]
Figure 2 (A) MGC-803 cells that were transfected with precursor miR-216a (pre-miR-216a) or scrambled controls (miR-control) were subjected to qRT-PCR for miR-216a expression. [score:3]
miR-216a inhibits activation of JAK2/STAT3 pathway. [score:3]
Overexpression of miR-216a facilitates EMT and subsequently promotes metastatic behaviors of HCC and ovarian cancer cells [14, 15]. [score:3]
We found that JAK2 restoration promoted the phosphorylation of STAT3 and EMT process, and subsequently facilitated migration and invasion of miR-216a overexpressing MGC-803 cells (P<0.05, respectively, Figure 7A-7C). [score:3]
Functionally, we demonstrated that miR-216a suppressed migration, invasion and EMT process of GC cells in vitro and in vivo. [score:3]
Multivariate Cox regression analysis indicated that miR-216a expression was an independent risk factor for poor prognosis of GC patients (P=0.018, Table 2). [score:3]
The clinicopathological significance of miR-216a expression in GC patients was shown in Table 1. Low level of miR-216a notably correlated with lymph node metastasis, venous infiltration, invasive depth and advanced TNM stage (P<0.05, respectively). [score:3]
miR-216a suppresses EMT process of GC cells. [score:3]
On the other hand, SGC-7901 cells that were transfected with miR-216a inhibitors (anti-miR-216a) or scrambled controls (anti-control) were subjected to immunoblotting. [score:3]
HE staining revealed that miR-216a overexpression significantly reduced the number of metastatic nodes of MGC-803 cells in nude mice livers. [score:3]
miR-216a inhibits migration and invasion of GC cells. [score:3]
miR-216a suppresses liver metastasis of GC cells in mice. [score:3]
Thus, miR-216a underexpression potentially functions as a predictor for poor prognosis of GC patients. [score:3]
Association between the clinicopathological features and miR-216a expression in gastric cancer patients. [score:3]
We disclosed that the expression of miR-216a was restrained in GC. [score:3]
Figure 4 (A) MGC-803 cells that were transfected with precursor miR-216a (pre-miR-216a) or scrambled controls (miR-control) were subjected to immunoblotting for E-cadherin, N-cadherin and Vimentin expression. [score:3]
Clinical analysis revealed that miR-216a expression was an independent prognostic factor for predicting poor clinical outcome of GC patients. [score:3]
Previous data demonstrate that miR-216a is involved in tumor initiation and progression, and its underexpression contributes to poor clinical outcome and cellular malignant phenotypes of CRC, pancreatic cancer, glioma and oral squamous cell carcinoma [10- 13, 17]. [score:3]
In this study, JAK2 was identified as a direct target gene of miR-216a in GC cells by a luciferase reporter assay, which was consistent with the results in pancreatic cancer [13]. [score:3]
In conclusion, we demonstrate that the expression of miR-216a is restrained in GC tissues and cell lines. [score:3]
These findings suggest that miR-216a potentially plays an anti-metastatic role GC by targeting JAK2/STAT3 pathway. [score:3]
Furthermore, miR-216a prohibits invasion and migration of CRC cells in vitro, and restrains liver metastasis in vivo by targeting KIAA1199 [11]. [score:3]
The expression and prognostic value of miR-216a in GC. [score:3]
Figure 1 (A) The relative expressions of miR-216a in 90 pairs of GC tissues and matched noncancerous tissues. [score:3]
Moreover, we disclosed that the expressions of miR-216a were reduced in GC cell lines. [score:3]
miR-216a/217 overexpression induces EMT of hepatocellular carcinoma (HCC) cells and promotes recurrence and sorafenib resistance of HCC [15]. [score:3]
Furthermore, low expression of miR-216a correlated with poor prognostic features and conferred a reduced survival in GC patients. [score:3]
Thus, miR-216a exerts its anti-metastatic role probably by targeting JAK2/STAT3 pathway in GC cells. [score:3]
miR-216a overexpression was confirmed by the qRT-PCR results (P<0.05, Figure 2A). [score:3]
To date, the exact role of miR-216a in GC and its target genes are poorly elucidated. [score:3]
miR-216a overexpression led to reduced levels of JAK2, phophorylated STAT3, Slug, Snail and Twist in MGC-803 cells. [score:3]
Precursor miR-216a clones, miR-216a inhibitors and scrambled controls clones were purchased from Genecopoeia (Guangzhou, China). [score:3]
The expression of miR-216a was detected by qRT-PCR in GC and matched noncancerous tissues. [score:3]
The “low” versus “high” miR-216a expression was defined according to the cut-off values of miR-216a level which were defined as the median of the cohort of tested patients. [score:3]
In accordance, miR-216a knockdown promoted activation of JAK2/STAT3 pathway in SGC-7901 cells (P<0.05, respectively, Figure 6). [score:2]
miR-216a knockdown promoted migration and invasion of SGC-7901 cells (P<0.05, respectively, Figure 2E and 2F). [score:2]
These results indicate that miR-216a inversely regulates EMT process of GC cells. [score:2]
miR-216a knockdown promoted activation of JAK2/STAT3 pathway in SGC-7901 cells. [score:2]
Quantitative data suggested that the JAK2 expression in GC tissues with high miR-216 level was significantly decreased compared with those with low miR-216a level (P<0.05, Figure 5F). [score:2]
Subsequent study demonstrated that miR-216a expression was strongly reduced in GC cells (SGC-7901, MGC-803, MKN-28, and BGC-823 compared to GES-1 cells (P<0.05, respectively, Figure 1B). [score:2]
These data suggest that miR-216a exhibits an anti-metastatic role in the development of GC. [score:2]
Therefore, it is valuable to study the regulatory effects of miR-216a in EMT process and metastasis of GC cells. [score:2]
miR-216a retrains EMT process of GC cells. [score:1]
Next, we disclosed whether JAK2 mediated the role of miR-216a in migration, invasion and EMT process of GC cells. [score:1]
miR-216a restrains pancreatic tumor growth via inducing G2/M arrest and apoptosis by decreasing lncRNA MALAT1 [12]. [score:1]
MGC-803 cells that were transfected with precursor miR-216a or scrambled controls were injected through the tail vein of nude mice and cultivated for 9 weeks. [score:1]
In contrast, no changes in relative luciferase activity were observed when the miR-216a binding site was mutated. [score:1]
Thus, the underlying mechanisms responsible for miR-216a underexpression require further investigation. [score:1]
In this study, we were aimed to investigate the expression and biological function of miR-216a in GC. [score:1]
Next, to determine the role of miR-216a in GC cells, we transfected MGC-803 cells with precursor miR-216a and scrambled controls (miR-control), respectively. [score:1]
Altogether, our data indicate that miR-216a plays an anti-metastatic role in GC cells. [score:1]
In contrast, no changes in relative luciferase activity were observed when the miR-216a binding site was mutated (Figure 5D). [score:1]
org), and the putative complementary sequence of miR-216a was identified in the 3′-UTR of JAK2 mRNA, as illustrated in Figure 5A. [score:1]
In addition, liver metastasis mo del showed that miR-216a overexpresion significantly reduced the number of metastatic nodules in livers arising from nude mice (P<0.05, Figure 3). [score:1]
Representative IHC data showed that strong staining of JAK2 was observed in GC tissues with low miR-216a level, while weak signal of JAK2 was detected in cases with high miR-216a level (Figure 5F). [score:1]
On the contrary, miR-216a facilitates epithelial-mesenchymal transition (EMT) of ovarian cancer cells and subsequently promotes migration and invasion of tumor cells [14]. [score:1]
The JAK2 levels in high-miR-216a PADCs were significantly lower than that of those low-miR-216a GCs. [score:1]
Figure 5 (A) The potential miR-216a binding site in wild type (wt) 3’-UTR sequence of JAK2. [score:1]
Figure 6MGC-803 cells that were transfected with precursor miR-216a (pre-miR-216a) or scrambled controls (miR-control) were detected by immunoblotting. [score:1]
As shown in Figure 5D, cells transfected with wt JAK2 3′-UTR vector containing a precursor miR-216a showed significantly lower luciferase activity than cells transfected with miR-control (P<0.05). [score:1]
, (Guangzhou, China) Small nuclear RNA U6 and GAPDH mRNA were used as internal controls for calculating the relative expression levels of miR-216a and JAK2 via the 2 [-ΔΔCt] method. [score:1]
MGC-803 cells that were transfected with precursor miR-216a (pre-miR-216a) or scrambled controls (miR-control) were intravenously injected into tail vein in nude mice. [score:1]
Subsequently, Spearman correlation analysis revealed that JAK2 mRNA levels were negatively correlated with miR-216a levels in GC tissues (r=-0.529, P=0.006, Figure 5E). [score:1]
Accordingly, we demonstrated that JAK2 restoration abrogated the anti-metastatic effects of miR-216a on GC cells with enhanced migration, invasion and EMT progression. [score:1]
MGC-803 cells that were transfected with precursor miR-216a (pre-miR-216a) or scrambled controls (miR-control) were detected by immunoblotting. [score:1]
These studies suggest that the role of miR-216a is a controversial topic in different cancers. [score:1]
In addition, GC patients with low miR-216a level showed a significant shorter survival (P<0.05, Figure 1C). [score:1]
Figure 3MGC-803 cells that were transfected with precursor miR-216a (pre-miR-216a) or scrambled controls (miR-control) were intravenously injected into tail vein in nude mice. [score:1]
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2
[+] score: 125
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-16-2, hsa-mir-216b
miRNA-216a was significantly upregulated and contributed to early hepatocarcinogenesis through suppressing the gene expression of tumor suppressor in lung cancer-1 (TSLC1) [19], which was in accordance with Xia et al. 's report that miRN-216a could induce epithelial-mesenchymal transition by targeting PTEN and SMAD7, thus contributing to hepatocarcinogenesis and recurrence [20]. [score:12]
Results revealed that patients with lymph node metastasis showed significantly lower miRNA-216b expression level than patients without lymph node metastasis (0.068 ± 0.054 versus 0.134 ± 0.117, P = 0.0168) (Figure 3(b)), while the miRNA-216a expression level showed no significant difference (P = 0.0845) (Figure 3(a)); patients with TNM IV showed significantly lower miRNA-216a expression level than patients with TNM 0-I or TNM II (0.039 ± 0.022 versus 0.088 ± 0.062, P < 0.05; 0.039 ± 0.022 versus 0.086 ± 0.065, P < 0.05) (Figure 3(c)); and patients with TNM III showed significantly lower miRNA-216b expression level than patients with TNM 0-I (0.072 ± 0.067 versus 0.134 ± 0.119, P < 0.05) (Figure 3(d)). [score:9]
Decreased expression of miRNA-216a was found in NSCLC patients' specimens and by directly targeting eIF4B and ZEB1, miRNA-216a could inhibit NSCLC cell growth and metastasis [17]. [score:8]
miRNA-216a was found to be downregulated in non-small-cell lung cancer (NSCLC) [17] and oral squamous cell carcinoma (OSCC) [18], while it was found to be upregulated in hepatocellular carcinoma (HCC) [19, 20]. [score:7]
Among the 21 patients who underwent esophagectomy, the number (proportion) of patients with upregulated miRNA-216b expression after esophagectomy was 19 (90.5%), while the number (proportion) was only 14 (66.7%) for miRNA-216a. [score:6]
Although the expression level of plasma miRNA-216a was also upregulated after esophagectomy, the result was insignificant (P = 0.2619) (Figure 2(a)). [score:6]
As shown in Figure 1, the expression level of miRNA-216a/b was significantly downregulated in ESCC patients compared with that of healthy controls (0.068 ± 0.052 versus 0.179 ± 0.098, P < 0.0001; 0.091 ± 0.087 versus 0.199 ± 0.161, P < 0.0001) (Figures 1(a) and 1(b)). [score:5]
In our study, the expression level of plasma miRNA-216a in postoperative samples was indeed upregulated compared with that of preoperative samples (0.118 ± 0.028 versus 0.101 ± 0.056), although it was insignificant (P = 0.2619). [score:5]
Plasma miRNA-216a/b were found to be considerably upregulated in the mo del of acute pancreatitis and were more specific than amylase and lipase in the detection of acute pancreatitis [23, 24], providing novel biomarkers for pancreatic injury. [score:4]
Downregulation of Plasma miRNA-216a/b in ESCC Patients. [score:4]
If we expanded the sample size, miRNA-216a would probably exhibit significant upregulation. [score:4]
Decreased expression of miRNA-216a in feces might be used as potential screening biomarkers for pancreatic cancer [25]. [score:3]
For example, overexpression of miRNA-216a could induce resistance of sorafenib in HCC cells [20]. [score:3]
What is more, the diagnostic value of miRNA-216a/b was also demonstrated in several diseases including acute pancreatitis [23, 24], pancreatic cancer (PCA) [25], and HCC [22]. [score:3]
Paired t-test was performed to analyze the difference of plasma miRNA-216a/b expression level between preoperative and postoperative samples. [score:3]
The qRT-PCR method was performed to detect the expression level of plasma miRNA-216a/b in 120 ESCC patients and 51 healthy controls. [score:3]
Influence of Operation on the Expression Level of Plasma miRNA-216a/b in ESCC Patients. [score:3]
In contrast with the tumor suppressive role of miRNA-216a/b mentioned above, the following studies held the opposite opinion. [score:3]
As a homologous miRNA of miRNA-216b, theoretically, miRNA-216a is expected to exhibit similar expression after esophagectomy. [score:3]
Despite the meaningful value of miRNA-216a/b in the diseases mentioned above, there has been no research on the role of miRNA-216a/b in ESCC up to now. [score:3]
miRNA-216a/b, two members of miRNA-216 family, have been demonstrated to be dysregulated in several types of human cancers. [score:2]
Recently, miRNA-216a/b, as two members of miRNA-216 family, have been demonstrated to be dysregulated in several types of human cancers. [score:2]
In the present study, we discovered, for the first time, that patients with ESCC had significantly lower plasma miRNA-216a/b expression level compared with healthy controls. [score:2]
Dysregulation of miRNA-216a/b was correlated with the lymph node metastasis and TNM stage of ESCC patients, thus indicating that they might be involved in the progression of ESCC. [score:2]
In order to have a better understanding of the role of miRNA-216a/b in ESCC, further efforts are recommended to reveal the exact mechanism of miRNA-216a/b in the carcinogenesis of ESCC. [score:1]
ROC curve analysis showed that plasma miRNA-216a/b exhibited satisfactory diagnostic value for ESCC, with AUC of 0.877 (95% CI: 0.818–0.922) for miRNA-216a and 0.756 (95% CI: 0.685–0.819) for miRNA-216b, which were higher than conventional biomarkers such as SCC-Ag (AUC: 0.665) and CEA (AUC: 0.549) reported in other studies [13, 16]. [score:1]
We found that plasma miRNA-216a/b could differentiate ESCC patients from healthy controls, with an AUC of 0.877 (95% CI: 0.818–0.922) for miRNA-216a and 0.756 (95% CI: 0.685–0.819) for miRNA-216b, respectively. [score:1]
The present study was designed to examine the expression of plasma miRNA-216a/b in ESCC patients and evaluate their diagnostic value, hoping to provide some valuable information in the early diagnosis of ESCC. [score:1]
Similar roles and mechanism of miRNA-216a were also found in OSCC [18]. [score:1]
We analyzed the correlation of plasma miRNA-216a/b expression level with the clinicopathological characteristics of 120 ESCC patients. [score:1]
Firstly, the sample size in our study was relatively small and only cross-sectional samples were used to compare the difference of plasma miRNA-216a/b between ESCC patients and healthy controls, which might result in bias in the final results. [score:1]
Additionally, miRNA-216a/b might influence the therapeutic effect of different treatments, thus providing candidate therapeutic methods for different cancers. [score:1]
Therefore, the prognostic value of plasma miRNA-216a/b was unknown. [score:1]
The possible reason is due to heterogeneous distribution of miRNA-216a in the study subjects after esophagectomy. [score:1]
In the recent years, the diagnostic value of miRNA-216a/b has drawn more and more attention. [score:1]
Plasma miRNA-216a was superior to miRNA-216b in the diagnosis of ESCC (z = 3.141; P = 0.0017) (Figure 4). [score:1]
Despite these findings, the role of miRNA-216a/b in ESCC has never been reported previously. [score:1]
In conclusion, our study demonstrated that plasma miRNA-216a/b might act as potential diagnostic biomarkers for ESCC. [score:1]
Further analysis revealed that plasma miRNA-216a/b were inversely correlated with lymph node metastasis and TNM stage, indicating that miRNA-216a/b might be involved in the progression of ESCC. [score:1]
Our results revealed that plasma miRNA-216a/b might serve as potential diagnostic biomarkers for ESCC. [score:1]
The Diagnostic Value of Plasma miRNA-216a/b for ESCC. [score:1]
At the cut-off value of 0.070, the sensitivity was 80.0% and the specificity was 90.2% for miRNA-216a; and at the cut-off value of 0.060, the sensitivity was 55.8% and the specificity was 90.2% for miRNA-216b. [score:1]
Therefore, it might be the small sample size that resulted in the inconformity between miRNA-216a and miRNA-216b. [score:1]
Secondly, miRNA-216a/b seem not to be specific miRNAs in ESCC. [score:1]
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3
[+] score: 102
Our in silico analysis revealed that miR-216 and miR-217 potentially target many important genes that play critical roles during the pathogenesis of PC (Table 1); and the downregulation of miR-217 [45] and miR-216 [44] suggests their potential as tumor suppressors in PC by targeting downstream targets, particularly the Kras oncogene [43] and Janus kinase 2 [44]. [score:12]
At 30 weeks of age, the expression of miR-216 (p-value = 0.016), miR-217 (p-value = 0.0078), miR-150 (p-value =0.023), Let-7b (p-value = 0.031,) and miR-96 were significantly downregulated, whereas the expression of miR-146b (p-value = 0.0078), miR-205, (p-value - 0.0078), miR-21, miR-195 (p-value = 0.031), and miR-34c (p-value = 0.063) were significantly upregulated in KC animals compared to control animals (Figure 2B). [score:10]
The expression of miR-223, miR-483-3p (p-value = 0.01), 146b, 205 (p-value = 0.001), 221, 21 (p-value = 0.023), 195, 34c and miR-26a (p-value = 0.0078) were significantly upregulated, whereas the expression of miR-216, miR-141, miR-217, Let-7b (p-value = 0.001), and Let-150 (p-value = 0.01) were significantly downregulated in human PC tissues as compared to the cancer-adjacent normal tissues (Figure 3E). [score:10]
At 40 weeks of age, the expression of miR-216, miR-217, miR-223, miR-141, miR-483-3p (p-value = 0.031), miR-195, Let-7b (p-value = 0.063) and miR-96 were significantly downregulated; on the other hand, the expression of miR-21, miR-205, miR-146b (p-value = 0.031), and miR-34c (p-value = 0.063) were upregulated in KC mice compared to the control animals (Figure 2C). [score:10]
The panel of differentially expressed miRNAs were validated by real-time PCR using TaqMan assays, and the results were consistent with the data that showed up-regulation of miR-21, miR-221, miR-100 and miR-26a and down-regulation of miR-26b, miR-141, miR-96, miR483-3p, miR-216, and miR-217 in the KC compared to control mice (Figure 1A). [score:7]
In addition to KC mice, we also observed a significant downregulation of miR-216 and miR-217 in human PC tissue (Figure 3E); these results are in agreement with earlier studies on human PC [38– 43] that show downregulation of miR-217 in 76.2% (16/21) of PC tissue as well as cell lines [43]. [score:7]
We have shown that in tumor samples compared to normal samples, the majority of miRNAs (miR-216, miR-217, miR-100, miR-345, miR-141, miR-483-3p, miR-26b, miR-150, Let-7b, Let-195 and miR-96) were downregulated, and few were upregulated (miR-146b, miR-205, miR-31, miR-192, miR-194 21, miR-379, miR-431, miR-541, and miR-199b). [score:6]
Similarly, the expression of miR-216 is significantly downregulated in PC [44]. [score:6]
The analysis for the KC animals compared to controls revealed that miR-150, miR-494, miR-138, miR-148a*, miR-216a, and miR-217 (p-value = 0.01) were significantly downregulated (Table 1), whereas, miR-146b, miR-205, miR-31, miR-192, and miR-21 (p-value = 0.01) were significantly upregulated (Table 2). [score:6]
Several studies have shown the abnormal expression of miRNAs including miR-21, Let-7b, miR-100, miR-217, and miR-216 in PC and have proposed them as candidates for early diagnosis and potential molecular targets [23, 24]. [score:5]
The expressions of miR-216 and miR-217 were also progressively reduced in KC mice, but the expressions of miR-21, miR-205, miR-146b, miR-34c, and miR-223 progressively increased (Figure 1A, 2A– 2D). [score:5]
The expression of pancreas-specific tumor suppressors miR-217 and miR-216 were unaltered at 10 weeks of age (presence of PanIN-Ia and Ib), but progressively decreased from 25 – 50 weeks of age as PanIN lesions progressed to PDAC. [score:5]
Both miR-216 and miR-217 act as potential tumor suppressors for PC by targeting the Kras oncogene [43]. [score:5]
Further, at 50 weeks of age, the expression of miR-216, miR-217, miR-345, miR-141, miR-483-3p, miR-26b, miR-96, Let-7b (p-value = 0.01), miR-100, miR-26a and miR-150 (p-value = 0.094) were further downregulated in KC animals compared to control mice (Figure 2D). [score:5]
On the other hand, miR-146b, miR-34c, miR-223, miR-195 (p-value = 0.031) and miR-216 (p-value = 0.063) were downregulated in KC mice compared to control littermates. [score:3]
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4
[+] score: 80
Figure 2Expression levels of miR-216 family membersExpression levels of miR-216 family members in clinical specimens and PDAC cell lines were determined using qRT-PCR. [score:5]
Transcription of all members of the miR-216 cluster was significantly reduced in PDAC specimens, and ectopic expression of these miRNAs suppressed cancer cell aggressiveness. [score:5]
Other study showed that significantly downregulation of miR-216a and miR-217 was detected in Kras [G12d];Pdx1-Cre mouse at 25 weeks [36]. [score:4]
In conclusion, downregulation of 4 clustered miRNAs (miR-216a-5p, miR-216a-3p, miR-216b-5p and miR-216b-3p) was detected by RNA sequencing -based miRNA signature analysis. [score:4]
Expression levels of the miR-216 family in PDAC specimens and cell lines. [score:3]
Among the miR-216 family, miR-216b-3p markedly inhibited PDAC cell aggressiveness (Figure 3). [score:3]
To elucidate molecular mechanisms of low expression of the clustered miRNAs, miR-216a-5p, miR-216a-3p, miR-216b-5p and miR-216b-3p in PDAC cells, PANC-1 and SW1990 cells were treated with the demethylating agent [5-aza-2’-deoxycytidine (5-aza-dC)]. [score:3]
In that study, 3 miRNAs (miR-216a, miR-216b, and miR-217) were reduced in expression in the Kras [G12D] pancreas. [score:3]
Moreover, expression levels of miR-216a-5p, miR-216a-3p and miR-216b-5p were same levels of mock and miRNA control transfectants (Supplementary Figure 2). [score:3]
Expression of miR-216-3p levels were significantly higher than those of mock and miRNA control transfected cells (Supplementary Figure 2). [score:3]
Expression levels of the miR-216 family in PDAC specimens and cell linesWe evaluated expression levels of the miR-216 family in PDAC tissues (n = 24), normal pancreatic tissues (n = 14) and two PDAC cell lines (PANC-1 and SW 1990). [score:3]
It was not recognized the significant relationships between any of the clinical parameters (i. e., TNM stage, metastasis or survival rate) and expression levels of any member of the miR-216 -family (data not shown). [score:3]
Patient clinicopathological features are summarized in Table 1. The expression levels of miR-216a-5p, miR-216a-3p, miR-216b-5p and miR-216b-3p were significantly lower in tumour tissues than in normal pancreatic tissues (Figure 2). [score:3]
Expression levels of miR-216 family members in clinical specimens and PDAC cell lines were determined using qRT-PCR. [score:3]
Expression levels of miR-216 family members. [score:3]
Expression of miR-216 family members and the effects on cell growth, migration and invasion in PDAC cell lines. [score:3]
Expression of miR-216 family members and the effects on cell growth, migration and invasion in PDAC cell linesThe functional roles of the miR-216 -family were performed by using restoration of mature miRNAs assays. [score:2]
Present results suggested that the miR-216 family could have anti-tumour functions in PDAC cells. [score:1]
Effects of miR-216a-5p, miR-216a-3p, miR-216b-5p and miR-216b-3p transfection into PDAC cells. [score:1]
Past studies showed that guide strands of miR-216a-5p and miR-216b-5p acted as anti-tumour miRNAs in several cancers [29, 30]. [score:1]
Pre-miR [™] miRNA precursors for miR-216a-5p (product ID: PM10545; Thermo Fisher Scientific), miR-216a-3p (product ID: PM24316), miR-216b-5p (product ID: PM12302), miR-216b-3p (product ID: PM28358), negative control miRNA (product ID: AM 17111), two FOXQ1 siRNAs (product IDs: s41290 and s41291) and control siRNA (product ID: D-001810-10) were purchased from Thermo Fisher Scientific. [score:1]
Schematic representation of the human miR-216 family in chromosomal location. [score:1]
Nevertheless, our present data showed that passenger strands miR-216a-3p and miR-216b-3p have anti-tumour functions in PDAC cells. [score:1]
In contrast, seed sequences of miR-216a-3p and miR-216b-3p are independent sequences. [score:1]
Because the role of the miR-216 cluster had not been reported in PDAC, we focused on it in further studies. [score:1]
Here, we showed that the clustered miR-216 family has anti-tumour activity in PDAC. [score:1]
Likewise pre- miR-216a, miR-216b-5p (guide strand) and miR-216b-3p (passenger strand) are derived from pre- miR-216b. [score:1]
We found that miR-217, miR-216a-5p/-3p and miR216b-5p/-3p were close together and were defined as clustered miRNAs. [score:1]
As shown in Figure 1, miR-216a-5p/-3p and miR216b-5p/-3p are located within the same chromosomal region (2q16.1). [score:1]
Those results suggest that the miR-216 family is important in PDAC oncogenesis. [score:1]
The miR-216 family members and miR-217 are located on human chromosome 2q16.1. [score:1]
Seed sequences of miR-216a-5p and miR-216b-5p are identical. [score:1]
Mature miRNAs, miR-216a-5p (guide strand) and miR-216a-3p (passenger strand) are derived from pre- miR-216a. [score:1]
We hypothesized that passenger strand of miR-216-3p may be incorporated into and function as part of the RISC structure. [score:1]
On the other hand, the functional significance of passenger strands miR-216a-3p and miR-216b-3p has not been adequately analysed. [score:1]
This miRNA is located in the same genomic region as the miR-216 cluster. [score:1]
We further investigated the target genes of miR-216. [score:1]
Functional assays showed that proliferation, migration and invasion activities of cancer cells were significantly suppressed in miR-216a-5p, miR-216a-3p, miR-216b-5p and miR-216b-3p transfectants compared with mock or miR-control transfectants (Figure 3). [score:1]
Among them, we focused on 4 clustered miRNAs, miR-216a-5p, miR-216a-3p, miR-216b-5p and miR-216b-3p located on human chromosome 2p16.1. [score:1]
We evaluated expression levels of the miR-216 family in PDAC tissues (n = 24), normal pancreatic tissues (n = 14) and two PDAC cell lines (PANC-1 and SW 1990). [score:1]
After transfection with miR-216-3p, Ago2-bound miRNAs were isolated, and RT-qPCR was carried out to determine whether miR-216-3p bound to Ago2. [score:1]
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[+] score: 21
RT-PCR validated three significantly upregulated miRNAs and three significantly downregulated miRNAs namely miR-217, miR-216a, miR-216b, miR-146a, miR-509-3p and miR-211. [score:7]
For validation using RT-PCR, we chose three miRNAs (miR-217, miR-216a, and miR-216b) that were upregulated and three miRNAs (miR-146a, miR-509-3p, miR-211) that were downregulated by at least 6 standard deviations in tumor compared to control arrays. [score:6]
However, overexpression of miR-216a was shown to activate the PI3K/Akt and TGF-β pathways by targeting PTEN and SMAD7, contributing to hepatocarcinogenesis and tumor recurrence in heptaocellular carcinoma. [score:5]
MicroRNA-216a/217 -induced epithelial-mesenchymal transition targets PTEN and SMAD7 to promote drug resistance and recurrence of liver cancer. [score:2]
Both miR-216a and miR-216b are associated with various types of cancer in particular adenocarcinoma of the pancreas. [score:1]
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[+] score: 19
miRNA-216a targets BECLIN1 by directly interacting with its 3′-untranslated region to inhibit it [71]. [score:8]
Wang S. Chen X. Tang M. MicroRNA-216a inhibits pancreatic cancer by directly targeting Janus kinase 2Oncol. [score:5]
In pancreatic cancer, miRNA-216a is significantly downregulated and cells can antagonize death through BECLIN1 -mediated autophagy [71, 72]. [score:4]
Zhang X. Shi H. Lin S. Ba M. Cui S. MicroRNA-216a enhances the radiosensitivity of pancreatic cancer cells by inhibiting beclin-1 -mediated autophagyOncol. [score:2]
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[+] score: 13
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-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-99a, mmu-mir-127, mmu-mir-128-1, mmu-mir-136, mmu-mir-142a, mmu-mir-145a, mmu-mir-10b, mmu-mir-182, mmu-mir-183, mmu-mir-187, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-139, hsa-mir-10b, hsa-mir-182, hsa-mir-183, hsa-mir-187, hsa-mir-210, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-224, hsa-mir-200b, mmu-mir-302a, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-128-1, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-127, hsa-mir-136, hsa-mir-193a, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, 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-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-96, mmu-mir-98, hsa-mir-200c, mmu-mir-17, mmu-mir-139, mmu-mir-200c, mmu-mir-210, mmu-mir-216a, mmu-mir-219a-1, mmu-mir-221, mmu-mir-222, mmu-mir-224, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-200a, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-363, mmu-mir-363, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-18b, hsa-mir-20b, hsa-mir-452, mmu-mir-452, ssc-mir-106a, ssc-mir-145, ssc-mir-216-1, ssc-mir-217-1, ssc-mir-224, ssc-mir-23a, ssc-mir-183, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-128-1, ssc-mir-136, ssc-mir-139, ssc-mir-18a, ssc-mir-21, hsa-mir-146b, hsa-mir-493, hsa-mir-495, hsa-mir-497, hsa-mir-505, mmu-mir-20b, hsa-mir-92b, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, hsa-mir-671, mmu-mir-216b, mmu-mir-671, mmu-mir-497a, mmu-mir-495, mmu-mir-146b, mmu-mir-708, mmu-mir-505, mmu-mir-18b, mmu-mir-493, mmu-mir-92b, hsa-mir-708, hsa-mir-216b, hsa-mir-935, hsa-mir-302e, hsa-mir-302f, ssc-mir-17, ssc-mir-210, ssc-mir-221, mmu-mir-1839, ssc-mir-146b, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-128-2, ssc-mir-143, ssc-mir-10b, ssc-mir-23b, ssc-mir-193a, ssc-mir-99a, ssc-mir-98, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-142, ssc-mir-497, ssc-mir-195, ssc-mir-127, ssc-mir-222, ssc-mir-708, ssc-mir-935, ssc-mir-19b-2, ssc-mir-19b-1, ssc-mir-1839, ssc-mir-505, ssc-mir-363-1, hsa-mir-219b, hsa-mir-371b, ssc-let-7a-2, ssc-mir-18b, ssc-mir-187, ssc-mir-218b, ssc-mir-219a, mmu-mir-195b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-31, ssc-mir-182, ssc-mir-216-2, ssc-mir-217-2, ssc-mir-363-2, ssc-mir-452, ssc-mir-493, ssc-mir-671, mmu-let-7k, ssc-mir-7138, mmu-mir-219b, mmu-mir-216c, mmu-mir-142b, mmu-mir-497b, mmu-mir-935, ssc-mir-9843, ssc-mir-371, ssc-mir-219b, ssc-mir-96, ssc-mir-200b
Ssc-miR-216 and ssc-miR-217 were also located in the same genome loci in chromosome 3. Overexpression of has-miR-216a/217 activates the PI3K/Akt and TGF-β signaling pathways by targeting PTEN and SMAD7 in human hepatocellular carcinoma cells [54]. [score:5]
Additionally, ssc-miR-216, ssc-miR-217, ssc-miR-142-5p, ssc-miR-96-5p, ssc-miR-182 and ssc-miR-183 have higher expression levels in mpiPSCs than that in hpiPSCs (Fig 3A). [score:3]
Ssc-miR-216 was also highly expressed in mpiPSCs. [score:3]
MicroRNA-216a/217 -induced epithelial-mesenchymal transition targets PTEN and SMAD7 to promote drug resistance and recurrence of liver cancer. [score:2]
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[+] score: 13
Other miRNAs from this paper: hsa-mir-126, hsa-mir-216b
Simultaneously, αvβ1, FAK, and p38 siRNA reversed OBCM -inhibited miR-126 expression and promoter activity (Fig. 5E–F), indicating that osteoblast-derived WISP-1 suppresses miR-216 via the αvβ1/FAK/p38 pathway. [score:7]
Taken together, these data demonstrate that miR-216 directly represses VCAM-1 protein expression via binding to the 3′UTR of human VCAM-1 through the αvβ1/FAK/p38 signaling pathway. [score:4]
To examine whether miR-216 regulates the 3′UTR of VCAM-1, we constructed a luciferase-reporter vector harboring the 3′UTR of VCAM-1 mRNA and another vector containing the miR-216 -binding site. [score:2]
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[+] score: 12
Amylase and lipase increases were noted from 1–8 h in rats in both 15 and 50 μg/kg dose groups while pancreatic necrosis was noted at 8, 24 and 48 h. MiR-375-3p has been reported to be enriched in islets and the miRNA with the highest intra-islet expression [38] and in our study was increased from 4–24 h in the 15 and 50 μg/kg groups, returning to approximately vehicle level by 48 h. MiR-216a-5p and miR-217-5p remained elevated in the serum of rats longer than amylase or lipase and had a much greater dynamic range which could be advantageous if detection of pancreatic injury is not able to be examined at earlier time points. [score:3]
Based on these studies miR-216a-5p displayed the largest dynamic range and correlated well with amylase and lipase indicating that it is the best translatable miRNA biomarker that correlated to pancreatic injury from rat to dog. [score:3]
MiR-216a-5p, amylase and lipase were increased in the serum concurrently at 1 h, remained elevated until 8 h while miR-216a-5p remained elevated until 24 h. MiR-217-5p displayed similar kinetics to miR-216a-5p except miR-217-5p generally had a larger dynamic range and remained elevated until 48 h. Both miRs-216a-5p and 217-5p displayed much larger dynamic ranges than amylase or lipase and remained elevated longer. [score:1]
Finally, we determined that miR-216a-5p appears to perform as well or better as a marker of pancreatic injury than amylase, lipase or other pancreas enriched miRNAs in rat and dog caerulein toxicity studies. [score:1]
It is possible that additional pancreas specific and/or enriched miRNAs may supplement the interpretation of pancreatic injury or serve as better biomarkers than miR-216a-5p in pancreatic toxicity studies utilizing different pancreatic toxicants. [score:1]
MiR-216b displayed similar kinetics to miR-216a-5p, but with a reduced dynamic range while miR-217-5p displayed increases similar to amylase. [score:1]
MiR-141-3p and miR-216a-5p were increased beyond vehicle treated dogs and did not display consistent time dependent increases. [score:1]
miRNAs were dose dependently increased in the serum of dogs treated with 15 and 45 ug/kg of caerulein and correlated to amylase and lipase increases while miR-216a-5p remained elevated until 24 h. Values are normalized to vehicle and to the cel-miR-55-3p spike in Conserved pancreas tissue enriched miRNAs were examined in the rat and dog mo dels of caerulein pancreatic toxicity in order to begin to characterize miRNAs as species translatable serum based biomarkers of pancreatic injury (Table  2). [score:1]
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[+] score: 11
Other tissue-specific miRNAs identified by our analysis that were also reported to be tissue-specific in other species include: miR-122, a liver-specific miRNA that functions as a tumor-suppressor gene in hepatocellular carcinoma [29]; miR-216, a pancreas-enriched miRNA, which has been reported as a marker for acute phase pancreatic injury and whose down-regulation is thought to be crucial in the development of pancreatic cancer [30]; miR-150, which our analysis reported as enriched in lymph nodes, is known to be expressed in mature B and T cells and, in particular, to regulate differentiation and the cytolytic effector function in CD8+ T cells [31]. [score:10]
Endo K Weng H Kito N Fukushima Y Iwai N MiR-216a and miR-216b as markers for acute phased pancreatic injuryBiomed. [score:1]
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[+] score: 10
Therefore, miRNAs up-regulated in F50 cerebellum (e. g. miR-135a, miR-135b and miR-7, see Figure 2) and F100 cerebellum (e. g. miR-216a and miR-216) make promising candidates for developmental switches in the cerebellum. [score:5]
An interesting expression pattern is represented by miR-216a, miR-216b and miR-217 which were found to be exclusively expressed in the F100 cerebellum, implying that they are highly stage- and tissue-specific miRNAs. [score:5]
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[+] score: 10
Among the microRNAs highly expressed in the kidney [14, 15], several key microRNAs (miR-192, miR-200b, miR-200c, miR-216a, and miR-217) were upregulated in glomerular mesangium of diabetic mouse mo dels (type I (streptozotocin (STZ) -induced) and type2 (db/db)) (vide infra). [score:6]
miR-216a and miR-217 are downstream targets of miR-192 through Zeb1/2 mediated mechanisms [17]. [score:3]
Akt activation by miR-216a and miR-217 led to glomerular mesangial cell expansion and hypertrophy, another hallmark of diabetic nephropathy (Figure 2A). [score:1]
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13
[+] score: 9
Other miRNAs from this paper: hsa-mir-200b, hsa-mir-200c, hsa-mir-200a
Furthermore, the upregulation of the miR-216a/217 cluster, which targets PTEN [51, 52], downregulates PTEN and elicits epithelial-mesenchymal transition (EMT) and cancer stem-like properties in hepatocellular carcinoma [51]. [score:9]
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[+] score: 8
Other miRNAs from this paper: hsa-mir-217, mmu-mir-216a, mmu-mir-217, gga-mir-216a, gga-mir-217
KRAS is upregulated in different cancer types, and post-transcriptional regulation of KRAS via interaction with miR-216a/217 was reported in vitro (36). [score:5]
These (and even shorter) isoforms also are no longer responsive to the validated regulation of KRAS by miR-216a/217. [score:2]
The other variants with shorter 3′UTRs, however, loose between 16 and 36 potential miRNA binding sites, and among these are the experimentally validated binding sites of miR-216a and miR-217. [score:1]
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[+] score: 8
Serum was also analyzed by Q-RT-PCR for a panel of 20 tissue enriched and potential miRNA biomarkers, including those identified for liver (cfa-miR-122 and -885), heart/muscle (cfa-miR-1, -133, and -206), testis (miR-34b/c), pancreas (cfa-miR-216), brain (cfa-miR-212), and ubiquitously expressed cfa-miR-193b. [score:3]
Of these, only cfa-miR-216a correlated with observed expression in both mouse and rat pancreas [33]. [score:3]
A recent rat study demonstrated that plasma levels of miR-216a and miR-216b increased after pancreatic injury [34]. [score:1]
A total of 22 miRNAs (Additional file 6: Figure S5) were selected for qPCR validation including the following 14 biomarker candidates of organ toxicity: liver (cfa-miR-122 and -885), pancreas (cfa-miR-216a/b); heart (cfa-miR-499); muscle (cfa-miR-206); heart/muscle (cfa-miR-1, -133a/b, and -208); testis (cfa-miR-34b/c); and brain and sciatic nervous tissues (cfa-miR-212, -432, and -885), and 5 miRNAs reported in the literature (cfa-miR-21, -192, -193a/b, and -200). [score:1]
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[+] score: 8
miRNA Target Genes Pathways miR-128 ABCB9, BTG1, DSCR1, RASD1 ABC transporters General miR-136 GRN, PPP1R9B miR-147 HOXA1, PTGFRN miR-148 EGR3, SCN3A miR-181b IGF1R, NKX6-1 Adherens junction, Maturity onset diabetes of the, Focal adhesion, **Long term depression miR-196a ABCB9, CPB2, IRS1, MAPK10 ABC transporters General, Complement and coagulation cas, Adipocytokine signaling pathwa, Insulin signaling pathway, Type II diabetes mellitus, Fc epsilon RI signaling pathwa, Focal adhesion, **GnRH signaling pathway, **MAPK signaling pathway, Toll like receptor signaling p, Wnt signaling pathway miR-203 SARA1 miR-20 BTG1, SARA1, YWHAB Cell cycle miR-21 TPM1 mir-216 GNAZ **Long term depression miR-217 RHOA Adherens junction, Axon guidance, Focal adhesion, Leukocyte transendothelial mig, Regulation of actin cytoskelet, TGF beta signaling pathway, T cell receptor signaling path, Tight junction, Wnt signaling pathway miR-31 ATP2B2, DNM1L, EGR3, PPP1R9B, YWHAB **Calcium signaling pathway, Cell cycle miR-7 SLC23A2 miR-7b HRH3, NCDN, SLC23A2 **Neuroactive ligand receptor in b: miRNAs and their targets (from TargetScan and miRanda). [score:8]
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[+] score: 7
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-20a, hsa-mir-21, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-16-2, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-204, hsa-mir-205, hsa-mir-181a-1, hsa-mir-217, hsa-mir-223, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, 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-146a, hsa-mir-149, hsa-mir-150, 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-26a-2, hsa-mir-365a, hsa-mir-365b, hsa-mir-370, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-335, hsa-mir-133b, hsa-mir-451a, hsa-mir-146b, hsa-mir-494, hsa-mir-193b, hsa-mir-181d, hsa-mir-92b, hsa-mir-574, hsa-mir-605, hsa-mir-33b, hsa-mir-378d-2, hsa-mir-216b, hsa-mir-103b-1, hsa-mir-103b-2, 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, hsa-mir-451b, hsa-mir-378j
For example, miR-142-5p and miR-142-3p (hematopoietic system), miR-122 (liver), and miR-216 and miR-217 (pancreas) were highly expressed in these organs and less abundantly in HM [48, 177], suggesting that these HM microRNAs may originate from the maternal bloodstream to specifically target the development, growth and function of the corresponding organs in the HM fed infant. [score:6]
These include for example muscle miR-1 and miR-133 [173], brain miR-9 and miR-124a [178], pancreatic miR-216 and miR-217 [179], liver miR-122 [21, 173], blood cell miR-451 [180], and endothelial cell miR-126 [181]. [score:1]
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18
[+] score: 7
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-215, 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
When globally analyzed the relapse-related miRNAs-miR-7, miR-100, miR-216 and let-7i—were up-regulated, and miR-486, miR-191, miR-150, miR-487 and miR-342 were down-regulated in early relapse ALL patients [76]. [score:7]
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19
[+] score: 7
Furthermore, miRNAs are subject to complex regulatory mechanisms so it is not surprising to observe numerous miRNAs with discordant copy number and expression (such as miR-216). [score:4]
Two miRNAs, miR-218 and miR-216, were common to training and all test sets, however, only miR-218 demonstrated concordant loss of copy number and expression (Figure 1). [score:3]
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20
[+] score: 7
RXRβ and TRβ, which initiated the process of metamorphosis, were up-regulated, while their predicted interaction miRNAs (mfi-miR-133c, mfi-miR-25, mfi-miR-31a and mfi-miR-363–3p; mfi-miR-15a, mfi-miR-15b and mfi-miR-216) were down-regulated. [score:7]
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[+] score: 7
Importantly, miRNAs have been shown to mediate TGFB signaling in diabetic nephropathy, and several candidates, including miR-92, miR-192, miR-216a, miR-217, and miR-377 are upregulated in mesangial cells in response to either glucose or TGFB, and are also indirectly correlated with increased collagen and fibronectin expression [44], [45], [46], [47]. [score:7]
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[+] score: 7
For example, hsa-miR-216a, the miRNA with second best AUC value has been described to be downregulated in lung neoplasm and is likewise more than 2-fold downregulated in melanoma in our study [34]. [score:7]
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[+] score: 7
Moreover, miR-377 is up-regulated in human and mouse mesangial cells exposed to high-glucose levels and can lead to increased fibronectin production in DN [13], while miR-216a regulates the collagen type I alpha 2 gene through mechanisms involving inhibition of the RNA binding protein Ybx1 [26]. [score:7]
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24
[+] score: 6
Last hsa-miR-216 was upregulated in cancer patients as compared to patients diagnosed with pancreatitis, with sensitivity of 50% and specificity of 100%. [score:3]
We found that salivary hsa-miR-216 may help discriminate pancreatitis from PDAC, with excellent specificity (100%), but poor sensitivity (50%) (Table 3). [score:1]
In this pilot study, we found that four salivary miRNAs (hsa-miR-21, hsa-miR-23a, hsa-miR-23b and hsa-miR-29c) successfully segregated PDAC patients from cancer-free donors, while hsa-miR-210 and let-7c indicate pancreatitis and hsa-miR-216 discriminates pancreatitis from cancer. [score:1]
However, at this stage of this project, salivary testing failed to differentiate between pancreatitis and PDAC, as hsa-miR-216 is detected only in pancreatitis and not in cancer, but with poor sensitivity. [score:1]
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25
[+] score: 6
The microarray analysis revealed that there was a significant upregulation of miR-221, miR-24, and miR-29a in BCSCs and a down-regulation of miR-216a, miR-25, and let-7d compared to differentiated cells (Table 1). [score:6]
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26
[+] score: 6
miR-30 significantly correlated with GFR and no detectable expression of miR-216a and miR-217 was found in patient samples [36]. [score:3]
Chen et al. [36] selected the following candidate miRNAs based on a report on EMT and kidney disease [46]: miR-15a, miR-17-92, miR-21, miR-30, miR-192, miR-216a, miR-217, and miR-377 [36]. [score:3]
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27
[+] score: 5
41, 42 Several miRNAs, including miR-21, miR-216a, miR-217 and miR-494, have been shown to confer sorafenib resistance in HCC by inhibiting autophagy through targeting phosphatase and tensin homolog (PTEN). [score:5]
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28
[+] score: 5
Pten, the inhibitor of PI3K/AKT, was targeted by miR-216 and miR-217 and these miRNAs were also activated by Tgfb1 [46]. [score:5]
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29
[+] score: 5
Lee et al reported that miR-122a is specifically expressed in liver tissue while miR-216 and miR-217 are preferentially expressed in the pancreas [38]. [score:5]
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30
[+] score: 4
Phosphatase and tensin homolog (PTEM) also is validated as a functional target of miR-216a/217. [score:3]
In combination with PTEM and decapentaplegic homolog 7 (SMAP7), miR-216a/217 raises the stem-like cell population and promotes the metastatic ability of HCC cells through activating the PI3K/Akt and TGF- β pathways [53, 54]. [score:1]
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[+] score: 4
For example, the miRNAs miR-21, miR-153, miR-216a, miR-217, miR-494 and miR-10a-5p have been shown to be upregulated in sorafenib-resistant cells and to participate in the mechanisms that are underlying sorafenib resistance [193]. [score:4]
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32
[+] score: 4
Conversely, 15 miRNAs resulted downregulated in activated B cells: mir-483, mir-95, mir-326, mir-135a, mir-184, mir-185, mir-516-3p, mir-30b, mir-203, mir-216, mir-150, mir-182*, mir-141 and mir-211 (Table 3). [score:4]
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33
[+] score: 3
Indeed, a number of miRNAs including miR18a, miR155, miR130b, miR125, miR216a/217 have roles in maintaining HCC stemness by targeting genes like CDX2, GATA6, NLK and controlling key pathways required for stemness [8, 28]. [score:3]
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34
[+] score: 3
112408.134243 20477536 5. Olena AF Rao MB Thatcher EJ Wu SY Patton JG miR-216a regulates snx5, a novel notch signaling pathway component, during zebrafish retinal developmentDev. [score:3]
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35
[+] score: 3
For example, a therapy with the vector-encoded pair miR-15a and miR-16-1 has been proposed for the treatment of chronic lymphocytic leukaemia (CLL) [13]; The microRNA cluster miR-216a/217 was reported to target genes PTEN and SMAD7 to induce the epithelial-mesenchymal transition, which can promote the drug resistance and recurrence of liver cancer [14]. [score:3]
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36
[+] score: 3
Previous studies have reported that miR-216a, miR-216b, and miR-217 are specifically expressed in the pancreas; these miRNAs were useful as biomarkers for pancreatic injury [30]. [score:3]
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37
[+] score: 3
Other miRNAs from this paper: hsa-mir-31, hsa-mir-217, hsa-mir-489
miR-216a and miR-217 -induced EMT-stimulated drug resistance via targeting PTEN in hepatocellular carcinoma [28]. [score:3]
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38
[+] score: 3
In one study, they showed that the CD44 3′UTR serves as a competitor for hsa-miR-216a-5p, hsa-miR-330-3p, and and hsa-miR-608 to increase CD44 and CDC42 protein levels in the breast cancer cell line MT-1, resulting in inhibition of cell proliferation and tumor-formation, promotion of angiogenesis, and induction of apoptosis [39]. [score:3]
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39
[+] score: 2
By contrast, T- and B-cell regulatory miR-150 was not detected, and several tissue-specific miRNAs, such as miR-122 (liver), miR-216, miR-217 (pancreas) and miR-142-5p and miR-142-3p (hematopoietic cells), were barely detectable (Figure 1b). [score:2]
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40
[+] score: 2
Other miRNAs from this paper: mmu-mir-216a
Gong D. Cheng H. P. Xie W. Zhang M. Liu D. Lan G. Huang C. Zhao Z. W. Chen L. Y. Yao F. Cystathionine γ-lyase (CSE)/hydrogen sulfide system is regulated by miR-216a and influences cholesterol efflux in macrophages via the PI3K/AKT/ABCA1 pathway Biochem. [score:2]
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41
[+] score: 2
Other miRNAs from this paper: hsa-mir-25
The same group also showed that, in HCC, Smad7 is inversely related to miR-216a/217 cluster, a negative regulator of Smad7, which controls EMT and cell migration of HCC cells [61]. [score:2]
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42
[+] 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-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, 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-96, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-198, hsa-mir-129-1, 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-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-196a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-217, 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-1-2, hsa-mir-15b, hsa-mir-23b, 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-137, hsa-mir-138-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, 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-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-185, hsa-mir-195, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, 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-301a, hsa-mir-99b, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-365a, hsa-mir-365b, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-382, hsa-mir-383, hsa-mir-151a, hsa-mir-148b, hsa-mir-338, hsa-mir-133b, hsa-mir-325, hsa-mir-196b, hsa-mir-424, hsa-mir-20b, hsa-mir-429, hsa-mir-451a, hsa-mir-409, hsa-mir-412, hsa-mir-376b, hsa-mir-483, hsa-mir-146b, hsa-mir-202, hsa-mir-181d, hsa-mir-499a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-301b, hsa-mir-216b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-320e, hsa-mir-378c, 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
Ason et al. (2006) miR-7, miR-9, miR-34b, miR-96, miR-124a, miR-125b, miR-132, miR-181b, miR-182, miR-183, miR-184, and miR-204, miR-215, miR-216, miR-217 Zebrafish Microarray, ISH ? [score:1]
Soares et al. (2009) let-7a,b,c,f,i, miR-7b, miR-9-5p, miR-9-3p, miR-34b, miR-103, miR-107, miR-124a, miR-125a,b, miR-128, miR-129-3p, miR-132, miR-138, miR-181a,b, miR-216, miR-217, miR-219, and miR-375 Zebrafish Microarray, ISH ? [score:1]
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43
[+] score: 2
Other miRNAs from this paper: hsa-mir-21, hsa-mir-182
Accumulating evidence has also shown the involvement of miRNAs, including miR-21, miR-106-25 and miR-216a/217, in the regulation of SMAD7 (refs 52, 53, 54). [score:2]
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44
[+] score: 2
The miRNAs differentially regulated by prenatal stress includes miR-23a (up), miR-129-2 (up), miR-361 (down), let-7f (up), miR-17-5p (down), miR-98 (up), miR-425 (down), miR-345-5p (down), miR-9 (up), miR216-5p (up), miR-667 (up), and miR-505 (down) (Figure 3A). [score:2]
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45
[+] 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-21, hsa-mir-22, hsa-mir-25, hsa-mir-33a, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-141, mmu-mir-155, mmu-mir-10b, mmu-mir-129-1, mmu-mir-181a-2, mmu-mir-183, mmu-mir-184, hsa-mir-192, mmu-mir-200b, hsa-mir-129-1, mmu-mir-122, 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-183, hsa-mir-210, hsa-mir-181a-1, hsa-mir-217, hsa-mir-223, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-122, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-141, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-129-2, hsa-mir-184, 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-21a, mmu-mir-22, mmu-mir-96, mmu-mir-34a, mmu-mir-129-2, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-10a, mmu-mir-25, mmu-mir-210, mmu-mir-181a-1, mmu-mir-216a, mmu-mir-223, mmu-mir-33, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, mmu-mir-217, hsa-mir-200a, hsa-mir-34b, hsa-mir-34c, hsa-mir-375, mmu-mir-375, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-33b, mmu-mir-216b, hsa-mir-216b, mmu-mir-1b, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-129b, mmu-mir-216c, bbe-let-7a-1, bbe-let-7a-2, bbe-mir-10a, bbe-mir-10b, bbe-mir-10c, bbe-mir-125a, bbe-mir-125b, bbe-mir-129a, bbe-mir-129b, bbe-mir-133, bbe-mir-1, bbe-mir-183, bbe-mir-184, bbe-mir-200a, bbe-mir-200b, bbe-mir-210, bbe-mir-216, bbe-mir-217, bbe-mir-22, bbe-mir-252a, bbe-mir-252b, bbe-mir-278, bbe-mir-281, bbe-mir-33-1, bbe-mir-33-2, bbe-mir-34a, bbe-mir-34b, bbe-mir-34c, bbe-mir-34d, bbe-mir-34f, bbe-mir-375, bbe-mir-7, bbe-mir-71, bbe-mir-9, bbe-mir-96, bbe-mir-34g, bbe-mir-34h, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
In contrast, many phylogenetically conserved miRNAs, as well as miRNAs present in both chordates and vertebrates (for example, miR-216, miR-217, miR-22, miR-25, and miR-96), could be reliably traced back to B. belcheri (Gray). [score:1]
Based on the available nematode, fruitfly, zebrafish, frog, chicken, mouse, rat and human miRNA information [18], 45 conserved amphioxus miRNAs could be classified into three distinct groups: 23 miRNAs (let-7a, miR-1, miR-7, miR-9, and so on) were conserved throughout the Bilateria; 5 miRNAs (miR-252a, miR-252b, miR-278, miR-281 and miR-71) were homologous to invertebrate miRNAs; and 17 miRNAs (miR-141, miR-200a, miR-200b, miR-183, miR-216, miR-217, miR-25, miR-22, miR-96, and so on) were present both in chordates and vertebrates (Table S9 in). [score:1]
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46
[+] score: 2
Previous study reported that miR-216 and miR-217 promoted TGF β -induced MC hypertrophy in vitro by regulating PTEN 32. [score:2]
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47
[+] score: 1
For example, lncRNA RP23-298H6.1-001 hosts miR-216a and miR-217, all of which were induced by TGF-β1 in glomerular mesangial cells [110]. [score:1]
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48
[+] 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]
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49
[+] score: 1
Each poly-miRTS was either found in several alleles (e. g. miR-224 site in SLA-3), or in a single allele (e. g. miR-216 site in SLA-3: gb_EU432082.1 allele) (e. g. SLA-3: Figure 2). [score:1]
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50
[+] score: 1
The elements were predicted to bind the annotated miRNAs called MIR45, MIR166 and MIR216 [32]. [score:1]
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51
[+] score: 1
To date only few lncRNAs have been reported as hosts for some miRNAs under diabetic conditions, for e. g., RP23-298H6.1-001 hosting miR-216a and miR-217 (refs 6, 11, 28, 29, 30). [score:1]
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52
[+] score: 1
However, between LDM and PMM, there were only five miRNAs that exhibited different methylation levels in their promoter regions, including miR-378, miR-181c, miR-181d, miR-139 and miR-216 (Supplementary Table S5). [score:1]
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53
[+] score: 1
Six predicted interaction regions with miRNA families were found in the DIO2 sequence: miR-9, miR-29abcd, miR-30abcdef, miR-193, miR-203 and miR-216a. [score:1]
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