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24 publications mentioning hsa-mir-650

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-650. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 488
Also, our results reveal that upregulation of miR-650 could induce docetaxel resistance of LAD cells via regulating Bcl-2/Bax expression by targeting tumor suppressor ING4. [score:11]
In previous study, we have showed that upregulation of ING4 could significantly increase the apoptosis of docetaxel-resistant LAD cells, suggesting that downregulation of miR-650 could lead to the same apoptosis-inducing effect as upregulation of ING4. [score:10]
0072615.g001 Figure 1(A) Upregulation and downregulation of miR-650 expression. [score:9]
Then, according to the median miR-650 expression level (median=8.45, normalized to U6 snRNA), LAD cases were classified into two expression groups: high-miR-650 expression group (n=52) and low-miR-650 expression group (n=44). [score:9]
The targets of miR-650 were predicted through at least three databases (Pictarget, miRBas and TargetScan), and ING4 was selected as a putative target, which was also recently reported in gastric cancer [16]. [score:9]
In our previous study, we have reported that upregulation of ING4 could reverse the docetaxel resistance of docetaxel-resistant LAD cells, suggesting that upregulation of ING4 could mimic the effects of anti-miR-650 on the chemosensitivity of docetaxel-resistant LAD cells to docetaxel [15]. [score:7]
These data indicated that upregulation of ING4 was potentially involved in the apoptosis-promoting function of anti-miR-650, which could induce the caspase-3 -dependent apoptosis by way of regulating the expression of Bcl-2/Bax. [score:7]
Feng and colleagues reported that downregulation of N-myc downstream-regulated gene 2 (NDRG2) expression involving promoter methylation and microRNA-650 promoted colorectal cancer progression [23]. [score:7]
The online miRNA databases (TargetScan, miRBase, and PicTarget) were used for prediction of miR-650 target genes. [score:7]
The key finding of this study is that upregulation of miR-650 expression is correlated with LAD development and progression. [score:7]
By statistical analysis (Table 1), it was shown that the level of miR-650 expression was significantly correlated with lymph node metastasis and clinical stage of LAD patients (P=0.023 and 0.019, respectively), suggesting that high miR-650 expression group showed a higher incidence of lymph node metastasis (70.7%) and more advanced clinical stage (75.6%) than the low miR-60 expression group (51.2% and 40.0%, respectively). [score:7]
Furthermore, miR-650 could affect the chemosensitivity of LAD cells to docetaxel via regulating Bcl-2/Bax expression by directly targeting ING4. [score:7]
Next, we analyzed the effect of miR-650 on ING4 protein expression, and found that miR-650 mimics could lead to the decreased expression of ING4 protein in SPC-A1/DTX or H1299/DTX cells, while anti-miR-650 could induce the increased expression of ING4 protein (Figure 5D). [score:7]
In this study, it was found that docetaxel-resistant LAD cells transfected with miR-650 inhibitor presented with decreased expression of Bcl-2 protein and increased expression of Bax protein, and the decreased Bcl-2/Bax ratio led to the execution of apoptotic progression in docetaxel-resistant LAD cells. [score:7]
Our findings demonstrated that miR-650 confers the docetaxel chemoresistance of lung adenocarcinoma cells via regulating Bcl-2/Bax expression by targeting ING4. [score:6]
Compared with corresponding non-tumor tissues, 23 of 26 human LAD tissues (88.5%) showed that miR-650 was significantly upregulated 11.6-fold to 2.5-fold, but only 3 cases (11.5%) were downregulated in different degree. [score:6]
Upregulation of miR-650 could significantly reduce the expression of ING4 protein in SPC-A1 cells (P<0.05; Figure 8B). [score:6]
ING4 was significantly downregulated in docetaxel-non-responding LAD tissues and inversely correlated with miR-650 expression. [score:6]
ING4 is often downregulated in docetaxel-resistant LAD tissues and negatively correlated with miR-650 expression. [score:6]
In order to examine the correlation between the upregulation of miR-650 and the resistance of LAD cells to docetaxel, miR-650 inhibitor was transfected into docetaxel-resistant LAD cells. [score:6]
Thus, downregulation of miR-650 could reverse the resistance of docetaxel-resistant LAD cells to docetaxel by inhibiting cell growth. [score:6]
In this study, we determined the expression of miR-650 in LAD tissues, and found that miR-650 was upregulated in LAD tissues and correlated with advanced clinical stage and a higher incidence of lymph node metastasis in LAD patients. [score:6]
Because ING4 is the target of miR-650, immunohistochemistry was performed to detect the expression of ING4 in LAD tissues collected from patients who received docetaxel -based chemotherapy (n=44). [score:5]
Also, LAD patients with high-level miR-650 expression had a shorter median overall survival (12.5 months) than those with low-level miR-650 expression (28.3 months). [score:5]
We then further elucidated the possible mechanisms of chemosensitivity enhancement in LAD cells induced by miR-650 inhibitor or ING4 overexpression. [score:5]
To explore the association of miR-650 expression with the clinical outcome of LAD patients, the overall survival of LAD patients relating to miR-650 expression, status of tumor differentiation, lymph node metastasis and clinical stage was determined (Figure 1C). [score:5]
Also, we found that both anti-miR-650 and pcDNA/ING4 could increase the expression of cleaved caspase-3 in SPC-A1/DTX cells but had no effects on the expression of pro-caspase-3 protein (Figure 7C). [score:5]
Furthermore, the co-tramsfection could partially rescue the decreased expression of Bcl-2 protein and the increased expression of Bax protein in SPC-A1/DTX cells induced by anti-miR-650 (Figure S1D). [score:5]
Further, confirmed the decreased expression of Bcl-2 protein and the increased expression of Bax protein in anti-miR-650 or pcDNA/ING4 -transfected SPC-A1/DTX cells (Figure 7E), which led to a decrease in the cell antiapoptotic ability (Bcl-2/Bax ratio). [score:5]
As shown in Figure 8A, the expression of miR-650 was significantly upregulated in SPC-A1/pLMP-miR-650 cells compared with SPC-A1/pLMP-miR-NC cells (P<0.01). [score:5]
It was observed that the effects of ING4 overexpression on the chemoresistance of docetaxl-resistant LAD cells were similar to the effects of miR-650 inhibitor. [score:5]
As miRNAs function mainly through the inhibition of target genes, the targets of miR-650 that function in docetaxel-resistant LAD cells were further investigated. [score:5]
Thus, these data indicated that upregulation of miR-650 might be, at least in part, involved in human LAD development. [score:5]
Patients with a low level of miR-650 expression (HSCORE < 143.5) had a significantly longer progression-free survival (PFS) than did those with a high level of miR-650 expression (HSCORE ≥ 143.5) (P=0.0024; Figure 2B). [score:5]
At the same time, the expression of ING4 protein was negatively correlated with miR-650 expression in responding or non-responding LAD tissues. [score:5]
LAD patients with high-miR-650 expression (n=52) showed a significantly worse prognosis than those patients with low-miR-650 expression (n=44). [score:5]
Therefore, miR-650 might regulate other target genes which are involved in formation of chemoresistant types in LAD cells, which needs to be further elucidated in future. [score:4]
Collectively, these findings further suggest that ING4 is a functional and direct target gene for miR-650 in LAD cells. [score:4]
ING4 is a direct target of miR-650. [score:4]
Upregulation of miR-650 reduces the in vivo sensitivity of parental LAD cells to docetaxel. [score:4]
Site-directed mutagenesis of the miR-650 target-site in the ING4-3’-UTR was performed using the Quick-change mutagenesis kit (Stratagene, Hei delberg, Germany) and named ING4 3’-UTR (mut), in which ING4 3’-UTR (wt) was used as a template. [score:4]
Downregulation of miR-650 reverses the resistance of docetaxel-resistant LAD cells to docetaxel. [score:4]
Upregulation of miR-650 reduces the in vitro sensitivity of parental LAD cells to docetaxel. [score:4]
Then, to further confirm target specificity between miR-650 and ING4 in LAD cells, we performed luciferase reporter assay with a vector containing the putative ING4 3’-UTR target site downstream of the luciferase reporter gene, which was transfected into LAD cells. [score:4]
To further analyze the association of miR-650 expression with clinicopathological factors of LAD patients, qRT-PCR assay was performed to detect miR-650 expression in a total of 96 LAD cases. [score:4]
These data suggested that upregulation of miR-650 might be an important inducer of docetaxel resistance of LAD cells. [score:4]
Next, we testify whether docetaxel treatment could affect the expression of miR-650 in LAD cells. [score:3]
Recently, the abberant expression of miR-650 has been reported to be correlated with the aggressiveness of colorectal cancer, gastric cancer, and chronic lymphocytic leukemia cells [23, 24]. [score:3]
miR-650 mimics and inhibitors (anti-miR-650) were purchased from Shanghai Gene-Pharma Co (Shanghai, China), along with the negative controls (miR-NC mimics or anti-miR-NC). [score:3]
Correlation between miR-650 expression and the responses of LAD patients to docetaxel. [score:3]
In their studies, higher expression of miR-650 was found to be associated with a favorable CLL prognosis and influenced the proliferation capacity of B cells. [score:3]
0072615.g006 Figure 6(A) Western blot analysis of ING4 protein expression in anti-miR-NC or anti-miR650 -transfected SPC-A1/DTX cells or SPC-A1/DTX cells co -transfected with anti-miR650 and siRNA/NC or siRNA/ING4. [score:3]
from quantitative analysis of qRT-PCR indicated that high level of miR-650 expression was closely correlated with advanced clinical stage and a high incidence of lymph node metastasis in LAD patients. [score:3]
As shown in Figure 2C, the level of miR-650 expression in SPC-A1/DTX or H1299/DTX cells was significantly higher than that in parental SPC-A1 or H1299 cells (P<0.05). [score:3]
In contrast to miR-650, the relative expression level of ING4 protein in responding tumor tissues was significantly higher than that in non-responding tumor tissues (P=0.022; Figure 9B). [score:3]
Statistical analyses indicate that LAD patients with high expression of miR-650 have a poorer prognosis. [score:3]
Also, Mraz and colleagues showed that microRNA-650 expression is influenced by immunoglobulin gene rearrangement and affects the biology of chronic lymphocytic leukemia (CLL) [24]. [score:3]
Further, the inverse correlation between miR-650 and ING4 protein expression was verified by linear regression analysis (Spearman rank test r=-0.645; P=0.018) (Figure 9C). [score:3]
These data suggest that miR-650 will be a significant predictor of poor prognosis for LAD patients and be a potential target for chemosensitizing LADs. [score:3]
Effects of miR-650 expression on the survival pathway in SPC-A1/DTX cells. [score:3]
For the mutated construct, the miR-650 target site tgcctcca was substituted with a acgagaa fragment. [score:3]
Correlation between miR-650 expression and clinicopathological factors of LAD patients. [score:3]
Expression of miR-650 was negatively correlated with responses of LAD patients to docetaxel. [score:3]
The 3’-untranslated region (UTR) of ING4 gene stood out because of the presence of one evolutionarily conserved binding site (260~266bp) for miR-650, suggesting cooperative binding and biologically effective interactions. [score:3]
from flow cytometry ands indicated that miR-650 inhibitor could induce the increased capase-3 -dependent apoptosis. [score:3]
Association of miR-650 expression with clinicopathological factors of LAD patients. [score:3]
Also, the co-tramsfection could partially rescue the increased expression of cleaved caspase-3 protein and the enhanced activity of caspase-3 in SPC-A1/DTX cells induced by anti-miR-650 (Figure S1B-C). [score:3]
Also, siRNA/ING4 could partially rescue the growth inhibition of SPC-A1/DTX cells induced by anti-miR-650 (Figure 6B). [score:3]
More importantly, further analyses showed that the expression of miR-650 was correlated with the efficiency of chemotherapy. [score:3]
Base pairing between miR-650 and wild-type (wt) or mutant (mut) target site in the 3’-UTR of ING4 mRNA was shown in Figure 5B. [score:3]
Our data showed that the mean level of miR-650 expression in non-responding tumor tissues (n=19) was significantly higher than that in responding tumor tissues (n=25) (P<0.001; Figure 2A). [score:3]
By multivariate analysis of the prognostic factors, we confirmed that high miR-650 expression was an independent prognostic factor (unfavorable; risk ratio: 4.65; 95% confidence interval: 1.58-6.21; P=0.011), while lymph node metastasis was also an independent prognostic factor (P=0.028). [score:3]
It was found that the mean level of miR-650 expression in non-responding tumor tissues was significantly higher than that in responding tumor tissues. [score:3]
was performed to detect the effect of miR-650 expression on the growth of docetaxel-resistant LAD cells. [score:3]
0072615.g002 Figure 2(A) Relative expression levels of miR-650 was detected in docetaxel-sensitive (n=25) and insensitive (n=19) LAD tissues via qRT-PCR. [score:3]
To gain insight into the biological role of miR-650 in human LAD progression, we first detected the expression of miR-650 in 26 human LAD tissues and corresponding non-tumor tissues by qRT-PCR (Figure 1A). [score:3]
ING4 was a functional target of miR-650 in docetaxel-resistant LAD cells. [score:3]
Then, ROC curve analysis was performed to establish the optimal cutoff value for the HSCORE of miR-650 expression level, which yielded a value of 143.5 (data not shown). [score:3]
indicated that pcDNA/ING4 could reverse the decreased ING4 protein expression in SPC-A1 cells induced by miR-650 mimics (Figure 6D). [score:3]
MiR-650 and ING4 affects the apoptosis of docetaxel-resistant LAD cells by way of regulating Bcl-2/Bax expression. [score:3]
This study showed that high level of miR-650 expression was correlated with enhanced malignant potential and poor prognosis of LAD patients. [score:3]
By univariate analysis, lymph node metastasis (N [1]+N [2]+N [3]/N [0]), clinical stage (III+IV/I+II) and miR-650 expression (High/Low) were the prognostic factors to predict a poor prognosis (P=0.026, 0.012 and 0.008, respectively). [score:3]
It was found that siRNA/ING4 could reverse the increased ING4 protein expression in SPC-A1/DTX cells induced by anti-miR-650 (Figure 6A). [score:3]
An miR-650 mimic (100 nM) was transfected into SPC-A1 or H1299 cells, and miR-650 inhibitor (anti-miR-650, 200nM) was transfected into SPC-A1/DTX or H1299/DTX cells using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA) according to the manufacturer’s instruction. [score:3]
Also, high miR-650 expression was a poor prognostic factor for LAD patients. [score:3]
In gastric cancer, Zhang’ et al reported that microRNA-650 could target ING4 to promote gastric cancer tumorigenicity [25]. [score:3]
Further, we conducted luciferase reporter assay and Western blotting to confirm that ING4 was a direct and functional target of miR-650 in LAD cells. [score:3]
As miR-650 could reverse the resistance of docetaxel-resistant LAD cells to docetaxel and we confirmed that ING4 was a direct and functional target, we investigated the molecular mechanisms by which miR-650 and ING4 mediated the regulation of chemosensitivity of LAD cells. [score:3]
However, there were no significant differences between miR-650 expression and other clinicopathological facors, including gender, age, smoking condition, tumor differentiation and T-primary tumor (P=0.439, 0.861, 0.484, 0.502 and 0.851, respectively). [score:3]
Detection of miR-650 expression in LAD tissues and corresponding nontumor tissues. [score:3]
Thus, it was concluded that the expression of miR-650 in advanced LAD tissues might be negatively correlated with the response of patients to docetaxel -based chemotherapy. [score:3]
Thus, it was concluded that overexpression of miR-650 might be involved in docetaxel-resistant phenotypes of human LADs. [score:3]
However, there were no reports about the association of miR-650 expression with the chemoresistance of tumor cells. [score:3]
MiR-650 was significantly upregulated in LAD tissues. [score:3]
First, we analyzed the effect of miR-650 expression on apoptosis of SPC-A1/DTX cells, and showed that anti-miR-650 could induce the increased apoptosis of SPC-A1/DTX (Figure 7A). [score:3]
These data, together with further univariate and multivariate analyses, suggest that high expression of miR-650 might be a significant predictor of poor prognosis for LAD patients. [score:3]
In general, the mean expression level of miR-650 in LAD tissues was significantly higher than that in corresponding non-tumor tissues (P<0.01; Figure 1B). [score:3]
Likewise, silencing of ING4 could partially rescue the increased caspase-3 -dependent apoptosis and decreased Bcl-2/Bax ratio induced by miR-650 inhibitor. [score:3]
In the present study, we firstly showed that miR-650 was significantly upregulated in docetaxel-resistant LAD cells (SPC-A1/DTX and H1299/DTX) compared with in parental LAD cells (SPC-A1 and H1299). [score:3]
The miR-650 expression plasmid was generated by cloning the genomic pre-miR-650 gene, with a 300-bp sequence on each flanking side, into pLMP vector (Open Biosystems Inc. ) [score:3]
Furthermore, silencing of ING4 could partially rescue the effects of miR-650 inhibitor on the chemosensitivity of docetaxel-resistant LAD cells. [score:3]
These data strongly suggested that the miR-650 expression in LAD patients was closely related to a poor prognosis. [score:3]
To explore the correlation between miR-650 expression and the efficiency of chemotherapy, we analyzed the survival data in patients who received docetaxel -based adjuvant chemotherapy (n=44). [score:3]
In the present study, we found that the average level of miR-650 expression was significantly higher in LAD tissues as compared with paired adjacent nontumor tissues. [score:2]
0072615.g003 Figure 3(A) 48h after SPC-A1/DTX or H1299/DTX cells were transfected with anti-miR-650 (or anti-miR-NC), qRT-PCR assay was performed to detect the expression of miR-650. [score:2]
0072615.g004 Figure 4(A) 48h after SPC-A1 or H1299 cells were transfected with miR-650 mimics or miR-NC mimics, qRT-PCR assay was performed to detect the expression of miR-650. [score:2]
48h after transfection, qRT-PCR assay showed that the expression of miR-650 in miR-650 mimics -transfected SPC-A1/DTX or H1299/DTX cells could be significantly increased (P<0.01; Figure 4A). [score:2]
To further investigate whether miR-650 is an important regulator of acquired docetaxel resistance in LAD cells, qRT-PCR was performed to detect the expression of miR-650 in docetaxel-resistant and parental LAD cells. [score:2]
MiR-650 expression was an independent prognostic factor for LAD patients. [score:2]
Furthermore, we have investigated the functional role for miR-650 in LAD cells, and showed that miR-650 could contribute to docetaxel chemoresistance of LAD cells by post-transcriptionally downregulating ING4. [score:2]
Next, we investigated whether upregulation of miR-650 could affect the sensitivity of LAD cells to docetaxel. [score:2]
to generate plasmid pLMP-miR-650. [score:1]
0072615.g007 Figure 7(A) Flow cytometric analysis of apoptosis in anti-miR-NC or anti-miR-650 -transfected SPC-A1/DTX cells. [score:1]
The mock or stably transfected SPC-A1 cells (SPC-A1/pLMP-miR-650 and SPC-A1//pLMP-miR-NC) were suspended in 100 µL PBS and injected subcutaneously into the right side of the posterior flank of female BALB/c athymic nude mice (Department of comparative medicine, Jinling Hospital, Nanjing, China) at 5 to 6 weeks of age. [score:1]
Flow cytometric analysis showed that the co-tramsfection could partially rescue the increased apoptosis in SPC-A1/DTX cells induced by anti-miR-650 (Figure S1A). [score:1]
Luciferase activities of LAD cells transfected with ING4-wt construct were significantly lower after transfection of miR-650 mimics and were significantly higher after transfection of anti-miR-650, whereas those with ING4-mut construct showed no significant difference (Figure 5C). [score:1]
Meanwhile, anti-miR-650 could lead to the decreased colony formation capacity of SPC-A1/DTX or H1299/DTX cells (P<0.05; Figure 3C). [score:1]
Effect of anti-miR-650 on the in vitro sensitivity of docetaxel-resistant LAD cells to docetaxel. [score:1]
Likewise, pcDNA/ING4 could partially rescue the growth promotion and increased IC [50]-value of docetaxel in SPC-A1 cells induced by miR-650 mimics (Figure 6E-F). [score:1]
Next, pcDNA/ING4 vector was transfected into miR-650 mimics -transfected SPC-A1 cells. [score:1]
The miR-650 levels after treatment with docetaxel (5.0 µg/L) were increased in the parental SPC-A1 or H1299 cells, but not in the SPC-A1/DTX or H1299/DTX cells (Figure 2D). [score:1]
Meanwhile, siRNA/ING4 could also partially rescue the decreased IC [50]-value of docetaxel in SPC-A1/DTX cells induced by anti-miR-650 (Figure 6C). [score:1]
By modulating the miR-650 level in LAD cells, we revealed that miR-650 could mediate the docetaxel resistance of LAD cells both in vitro and in vivo. [score:1]
Next, we analyzed the changes of docetaxel sensitivity of chemoresistant LAD cells induced by anti-miR-650. [score:1]
siRNA/ING4 or pcDNA/ING4 could partially rescue the effects of anti-miR-650 or miR-650 mimics on the sensitivity of SPC-A1/DTX or SPC-A1 cells to docetaxel. [score:1]
Then, miR-650 mimics was transfected into parental SPC-A1 or H1299 cells. [score:1]
After transfected with anti-miR-650, SPC-A1/DTX cells were co -transfected with siRNA/ING4. [score:1]
These data support the notion that miR-650 could induced the increased docetaxel resistance of LAD cells in vivo. [score:1]
Also, using the, condensed and fragmented nuclei in anti-miR-650 -transfected SPC-A1/DTX cells were obviously observed (Figure 7B). [score:1]
Figure S1 ING4 was involved in the effect of miR-650 on apoptosis in SPC-A1/DTX cells. [score:1]
Comparison of the overall survival (OS) between low-miR-650(n=44) and high-miR-650(n=52) patients (P=0.008). [score:1]
Since the size of tissue sample in the present study is small, further investigation of a larger patient population will be necessary to confirm the association of miR-650 and its target ING4 with the responses of LAD patients to docetaxel -based chemotherapy. [score:1]
Effect of miR-650 mimics on the in vitro sensitivity of parental LAD cells to docetaxel. [score:1]
qRT-PCR for miR-650 was performed by using 26 human LAD tissues and corresponding adjacent normal tissues. [score:1]
48h after transfection, qRT-PCR assay showed that the expression of miR-650 in anti-miR-650 -transfected SPC-A1/DTX or H1299/DTX cells was significantly decreased compared with that in anti-miR-NC-transected cells (P<0.05; Figure 3A). [score:1]
Also, the IC [50]-value of docetaxel in SPC-A1/pLMP-miR-650 cells was modestly increased by approximately 53.4% (Figure 8C). [score:1]
The median survival time for the LAD patients with high-miR-650 was 12.5 months (95% CI: 9.5-15.7 months), and for LAD patients with low-miR-650 was 28.3 months (95% CI: 17.5-36.2 months; P=0.008). [score:1]
Additionally, the PFS of LAD patients with high-level miR-650 who received docetaxel -based chemotherapy was significantly lower than that of patients with low-level miR-650. [score:1]
To further investigate the possible effect of miR-650 expression on LAD cell sensitivity to docetaxel in vivo, SPC-A1 cells were stably transfected with pLMP-miR-650 or control pLMP-miR-NC vector. [score:1]
All DNA plasmids (pLMP-miR-650 or pLMP-miR-NC) for transfection were extracted by DNA Midiprep or Midiprep kit (Qiagen). [score:1]
Following docetaxel treatments, the tumors formed from SPC-A1/pLMP-miR-650 cells grew faster than those formed from SPC-A1/pLMP-miR-NC cells (P<0.05; Figure 8D). [score:1]
To further testify the roles of ING4 in miR-650 -induced chemoresistance of LAD cells, siRNA/ING4 was transfected into anti-miR-650 -transfected SPC-A1/DTX cells. [score:1]
To further investigate whether miR-650 expression might be a prognostic factor in LAD patients, univariate and multivariate data analyses were performed using the Cox proportional hazards regression mo del (Table 2). [score:1]
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2
[+] score: 21
Most recently, the PRR -mediated down-regulation of miR-650 was interestingly revealed to modulate the expression of several ISGs, including interferon regulatory factor 3 (IRF3), IFIT2 and MxA. [score:7]
Pichulik T. Khatamzas E. Liu X. Brain O. Delmiro Garcia M. Leslie A. Danis B. Mayer A. Baban D. Ragoussis J. Pattern recognition receptor mediated downregulation of microRNA-650 fine-tunes MxA expression in dendritic cells infected with influenza A virus Eur. [score:6]
In IAV-infected monocyte-derived dendritic cells (MDDCs), miR-650 directly targets the antiviral ISG MxA. [score:4]
They appeared to inhibit the viral infection (e. g., miR-4276 [60] and miR-650 [61]) or to facilitate (e. g., miR-451 [62] and miR-548an [63]) IAV replication (Figure 1 and Table 1). [score:3]
The virus -induced reduction of miR-650 leads to the increase of the MxA and the establishment of an antiviral state in host [61]. [score:1]
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3
[+] score: 19
The amplified chromosomal region included MIR650, which has among its targets the promoter region of the NDRG family member 2 (NDRG2) tumor suppressor gene where it has been reported to be able to repress NDRG2 gene expression at the transcriptional level in CRC [26]. [score:7]
The analysis of the prioritized genes harboring the loss-of-function variants combined with the ERBB2, AR, and MIR650 genes through IPA software revealed that 14 of the 16 genes were connected in a unique network, called the “Gene expression, cellular growth and proliferation, tissue development” network. [score:4]
The 13 genes exhibiting truncating variants were combined with the erb-b2 receptor tyrosine kinase 2 (ERBB2) gene harboring the rs1058808 single nucleotide polymorphism (SNP), which was predicted to be deleterious by the sorting intolerant from tolerant (SIFT) and polymorphism phenotyping version 2 (PolyPhen-2) tools, the microRNA-650 (MIR650) gene (a colorectal cancer-related gene), and the androgen receptor (AR) gene harboring the pathogenic rs9332969 SNP to test the putative enrichment of the canonical pathways, disease and biological functions, and molecular networks. [score:3]
From the literature, four of these six genes (CHMP2B, DENND2D, KALRN, and TGM4) have been previously identified as being involved in oncogenesis, while 3 (MIR650, ADHFE1, and MEP1A) may be related to CRC development and differentiation (see all the references in Additional file 8: Table S8). [score:2]
A microduplication of chromosome 22q11.22, encompassing MIR650 gene, previously related to CRC, was also detected. [score:1]
Significant gene association was observed only when the gene list was reduced to AR (mutated and causative of PAIS in the proband), MIR650 (already related to CRC pathogenesis and present in a rearranged chromosomal region), ERBB2 (determined to be functionally impaired by the candidate gene approach), and the 13 genes harboring truncating variants (identified by the whole-exome approach). [score:1]
The core molecular hub in this network is represented by seven genes (MIR650, alcohol dehydrogenase, iron containing 1 [ADHFE1], charged multivesicular body protein 2A [CHMP2B], DENN domain containing 2D [DENND2D], kalirin RhoGEF kinase [KALRN], meprin A subunit alpha [MEP1A], and transglutaminase 4 [TGM4]) connected with AR and ERBB2, revealing an altered cross-talk between these two signaling pathways. [score:1]
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4
[+] score: 19
All 6 miRNAs (hsa-miR-21-5p, hsa-miR-31-5p, hsa-146a-5p, hsa-miR-155-5p, hsa-miR-375 and hsa-miR-650) with increased expression in active UC demonstrated a similar upregulated expression profile in both active CDc and IC compared to healthy controls. [score:7]
In this study, we confirm the strong upregulation of hsa-miR-650 in active UC compared to both inactive UC (FC = 11.59) and controls (FC = 13.69) and a downregulation of hsa-miR-196b-5p in active UC vs. [score:6]
The miRNA microarray expression data was confirmed by performing qRT-PCR for hsa-miR-200c-3p and 10 other differentially expressed miRNAs selected because of their highly significant p-value or fold change (hsa-miR-21-5p, hsa-miR-31-5p, hsa-miR-146a-5p, hsa-miR-155-5p, hsa-miR-196b-5p, hsa-miR-196b-3p, hsa-miR-200b-3p, hsa-miR-375, hsa-miR-422a and hsa-miR-650). [score:5]
Iborra et al. reported hsa-miR-650 and hsa-miR-196b-5p as altered in active UC vs. [score:1]
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5
[+] score: 18
Most significantly down-regulated was hsa-miR-650 (p value of 4 × 10 [−23]), most significantly up-regulated was hsa-miR-3620-3p (p value of 6 × 10 [−19]). [score:7]
a The first miR-650 is only expressed in blood of strength athletes. [score:3]
The expression of miR-650 is exemplarily presented in Fig.   4a. [score:3]
The most significantly altered miR-650 was correlated to a range of different pathologies, including heart failure [28], congenital heart disease [29], diabetic ischemic heart failure [30] and different cancer types (gastric cancer [31], melanoma [32], leukemia [33], hepatocellular carcinoma [34], glioma [35], colorectal cancer [36] and lung cancer [37]). [score:3]
Similarly, the levels of miR-140-5p and miR-650, both of which have been reported as makers for a wide range of human pathologies significantly depend on the training mode. [score:1]
We found three correlations of the creatine kinase (CK) at day 5 with miR-18-3p, miR-33b-3p or miR-650. [score:1]
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[+] score: 12
The miRNAs that appear to directly target BIRC5 are miR-145-5p, miR-150-5p, miR-195-5p, and miR-650; both miR-145-5p and miR-150-5p were associated with better survival after diagnosed with CRC overall or with rectal cancer specifically when upregulated in CRC tumor tissue. [score:7]
The miRNAs identified in our study, miR-145-5p, miR-150-5p, miR-195-5p, miR-650, and miR-29b-3p, may serve as reasonable therapeutic targets given their likely role in influencing activity of BIRC5 and CASP7, two important elements in the apoptosis pathway. [score:3]
Several miRNAs were associated with multiple genes, including miR-150-5p with six genes (BIRC5, CSF2RF, TUBA1B, IRPR1, PIK3CD, and BCL2), miR-650 with five genes (BIRC5, CSF2RB, ITPR1, PIK3CD, and BCL2), miR-195-5p with three genes (BIRC5, TUB1B, and BCL2), and miR-20b-5p and miR-3124-5p each with two genes (miR-20b-5p with BIRC5 and CTSS and miR-3124-5p with TNFRSF10B and CSF2RB). [score:1]
Ten of the 14 miRNAs associated with BIRC5 has a seed-region match, and four of these matches, miR-145-5p, miR-150-5p, miR-195-5p, and miR-650, had a negative beta coefficient. [score:1]
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[+] score: 11
From our results the extrinsic pathway of apoptosis appeared more targeted in MMG than in 1 g. Indeed, miR-7, miR-7-1*, miR-144 and miR-650, which were anti-correlated to pro-apoptotic TNFRSF10B, were exclusively radio-responsive in MMG. [score:3]
Eight miRNAs (let-7i*, miR-7, miR-7-1*, miR-27a, miR-144, miR-200a, miR-598, miR-650), were differentially expressed only when PBL were incubated in MMG. [score:3]
Moreover, let-7i*, miR-7, miR-7-1*, miR-27a, miR-144, miR-200a, miR-598, miR-650 are deregulated by the combined action of radiation and MMG. [score:2]
Notably, pro-apoptotic BAX was anti-correlated to four miRNAs (miR-144, miR-200a, miR-598,miR-650) deregulated in only 2Gy MMG PBL. [score:2]
Except for miR-371-5p and miR-886-3p, which were differently altered in 1 g at 24 h after irradiation (Table 1), miR-99b, let-7i*, miR-144, miR-200a, miR-27a, miR-598, miR-650, miR-7, miR-7-1* were activated by the combined exposure to IR and MMG (Figure 4B). [score:1]
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[+] score: 10
In two different approaches researchers have shown an important role for the gene inhibitor of growth (ING4) which is targeted by hsa-miR-650 and hsa-miR-622 and this in turn, seems to be associated with increased invasion/migration of gastric cell lines in vitro and promote metastasis in nude mice (Zhang et al., 2010; Guo et al., 2011). [score:5]
So, there are miRNA profiles that promote tumor growth including hsa-miR-622, hsa-miR-650, hsa-miR-223, hsa-miR-21, and hsa-miR-181a, among others (Zhang et al., 2010, 2012a, b; Guo et al., 2011; Li et al., 2011b); while hsa-miR-107, -145, -495, -551a, let-7f, -218, and -610, among others, inhibit cell invasion and metastasis (Tie et al., 2010; Li et al., 2011a, 2012b; Liang et al., 2011; Feng et al., 2012; Gao et al., 2012; Wang et al., 2012). [score:3]
MicroRNA-650 targets ING4 to promote gastric cancer tumorigenicity. [score:2]
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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-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-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-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
This is in part explained by the fact that artificial miR-650 (MIMIC miR-650) reduced CLL cell proliferation through targeting cyclin -dependent kinase 1 (CDK1), inhibitor of growth 4 (ING4), and early B-cell factor 3 (EBF3) [22]. [score:5]
Higher expression of miR-650 and miR-708 has been associated with a favorable CLL prognosis [21] and affects B-cell proliferation [22]. [score:3]
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[+] score: 7
CNV region position genotypes CNV ID functional relevance expression (mimiRNA/[18] ) conservation mir-1977 chr1:556050-556128 chrM chr1:554403-560267 2,3,4 3.1 not reported/NA primates mir-1324 chr3:75762604-75762699 chr3:75464498-75782745 1,2 1432.2 not reported/NA primates mir-548i-2 chr4:9166887-9167035 chr4:9117494-9354801 1,2 1815.3 not reported/NA primates mir-1275 chr6:34075727-34075806 chr6:34071086-34077139 1,2 2853.12) upregulated in blood cells of MS patients [41] not reported/NA primates mir-1302-2 chr9:20144-20281 chr1, 15,19 chr9:485-38531 2,3 4134_full not reported/NA primates mir-1233 chr15:32461562-32461643 chr15 chr15:32450046-32662643 2,3,4,5 6351.3 1) not reported/NA primates mir-1233 chr15:32607783-32607864 chr15 chr15:32450046-32662643 2,3,4,5 6351.3 1) not reported/NA primates mir-650 chr22:21495270-21495365 chr22:20711019-21578950 0,1,2 8103_full 1) in several tissues (mostly ovary and ovary-derived cancers)/high primatesdupl. [score:6]
The number of observed copies ranged from 0 (e. g., hsa-mir-384 and hsa-mir-650) to 6 (e. g., hsa-mir-1268). [score:1]
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[+] score: 6
RAC2 had a seed-region match with miR-650, ROCK2 had a seed-region match with sevens, with miR-1243 and miR-204-3p expression being inversely related to ROCK2 expression; DAAM2 had seed region matches with fours and PRICKLE2 has a seed region match with threes. [score:5]
While 33s were associated with only one gene, manys were associated with multiple genes: miR-7i-5p, miR-133b, miR-221-3p, miR-27a-3p, miR-29a-3p, miR-6515-5p, miR-663a, and miR-93-5p were associated with two genes; miR-145-5p, miR-17-5p, miR-193-3p, miR-19b-30, miR-203a, miR-20a-5p, miR-21-5p, miR-3651, miR-650, and miR-663b with three genes, and miR-92a-3p, miR-150-5p, and miR-20b-5p with four genes. [score:1]
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12
[+] score: 6
Meanwhile, the over -expression of miR-650 may promote GC proliferation and growth of cancer cells, at least partially through directly targeting ING4 [31]. [score:6]
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[+] score: 5
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-215, 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-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
Tumor associated miRNAs present in this network included miR-18a, miR-93, miR-146b, miR-200c, miR-214, miR-223, miR-650 and miR-1285, collectively repressing 9 tumor suppressors genes (including ARID2, ATM, CYLD, KLF6, NBN, SDHD, SMAD4, SMARCA4, TNFAIP3), nine oncogenes (including BCL2, CREB1, CREBBP, FOXO1, MYC, MYH11, MYH9, NOTCH1), growth inhibitors (BMPR2, BTG2, BTG3, LITAF and PA2G4), chromatin remo delers, six claudin genes (CLDN11, CLDN14, CLDN5, CLDN7, CLDN8, CLDND1) 11 DNA-repair/ATM pathway genes (ATF4, CREB3, CREB5, DCLRE1C, ERCC1, PARP1, POLR2C, RAD23B, RAD51, RPA1, XRCC5) and six proapoptotic genes (BAK1, BCL2L1, MCL1, SMAD3, SMAD5, SMAD7). [score:5]
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[+] score: 4
Extracellular vesicles from cancer stem cells contained miR29a, miR650, and miR151, all associated with tumor invasion and metastases, along with miR19b, miR29c, and miR151, known to be up-regulated in patients with renal carcinomas (Grange et al., 2011). [score:4]
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[+] score: 4
For example, we previously identified a differential miRNA -expression profile between docetaxel-resistant and parental LAD cells, and showed that dysregulation of some miRNAs (miR-650, Let-7c, miR-200b and miR-100) was linked with the chemoresistance of LAD cells [9- 12]. [score:4]
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[+] score: 4
Our miRNA profile (84) Chromosomal localization Fold change Reference DOWNREGULATED hsa-miR-206 6p12.2 −7.53(29) hsa-miR-219-2-3p 9q33.3 −6.64(52) hsa-miR-383 8p22 −6.56(12, 55, 56) hsa-miR-138 16q13.3/3p21.32 −5.16(12, 14) hsa-miR-323-3p 14q32.2 −4.96(12, 52) hsa-miR-122 18q21.31 −4.82 hsa-miR-105 Xq28 −4.66 hsa-miR-129-5p 11p11.2/7q32.1 −4.56(23) hsa-miR-935 19q13.43 −4.53(52) hsa-miR-329 14q32.2 −4.48 hsa-miR-129-3p 11p11.2/7q32.1 −4.43 hsa-miR-650 22q11.21 −4.19 hsa-miR-184 15q24.3 −4.14 hsa-miR-370 14q32.2 −3.99(12) hsa-miR-433 14q32.2 −3.96(29) hsa-miR-138-2* 16q13. [score:4]
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[+] score: 3
1 (36.5 kb) gain DDX19A, DDX19B;16q23.1 (16.2 kb) loss WWOX 19q13.33 168753 M 61,936 Loss Maternal SHANK1, CLEC11A 4p15.33 (5.4 kb) loss not in any gene 20p13 92540L M 15,645 Loss Paternal SLC23A2 exonic2q34 (23 kb) loss SPAG16 22q11.21 118909L F 7277 LossUnknown [d] CECR2 exonic7q22.2 (12.4 kb) gain not in any gene;10q21.3 (8.1 kb) loss CTNNA3 22q11.22-q11.23 MM0177-3 M 656,280 Gain Maternal RAB36, FBXW4P1, RTDR1, GNAZ, MIR650, IGLL5, BCR − 22q11.23 154266L M 6784 Loss Maternal UPB1 11p14.3 (138.6 kb) loss not in any gene Xq28 100676L M 123,871 Gain Maternal ZNF185, CETN2, NSDHL 3q22.3 (11.5 kb) loss not in any gene;5p14.2 (12.2 kb) loss not in any gene;22q12.3 (35.6 kb) gain not in any gene ASD, autism spectrum disorder; CNV, copy number variations; F, female; M, male; qPCR, quantitative polymerase chain reaction; UTR, untranslated region. [score:3]
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[+] score: 3
It was also reported that miR-650 targets ING4 to promote gastric cancer tumorigenicity [31]. [score:3]
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[+] score: 3
Likewise severals were associated with multiple genes (miR-150-5p with eight genes, miR-195-5p with four genes, miR-203a with five genes, miR-20b-5p with four genes, miR-650 with six genes and miR-92a-3p with five genes). [score:1]
Interestingly, the six genes associated with miR-650 also were associated with miR-150-5p. [score:1]
Interestingly, six of these eights associated with miR-150-5p were also associated with miR-650. [score:1]
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[+] score: 2
Three of these genes had a seed region match for miR-150-5p (PDGFRA, RASGRP3, and PRKCB), whereas miR-650 only had a seed region match with PDGFRA. [score:1]
Both miR-150-5p and miR-650 were associated with the same 7 genes. [score:1]
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[+] 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-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-215, 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-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
Zhang X. Zhu W. Zhang J. Huo S. Zhou L. Gu Z. Zhang M. MicroRNA-650 targets ING4 to promote gastric cancer tumorigenicity Biochem. [score:2]
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While SNPs in hsa-mir-196a-2, hsa-mir-570, and has-mir-650 did not affect their cleavage site (Table 5). [score:1]
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[+] score: 1
Nineteen out of 21 patients present at least one CNV-miRNA; some miRNAs are present only in deleted (i. e., miRNA6891, miRNA4650-2, miRNA5007, miRNA12331-1, miRNA1233-2), some only in duplicated (miRNA3914-1, miRNA3914-2, miRNA6761, miRNA650, miRNA6817, miRNA1256) and some in both (miRNA3675, miRNA570; Tables 2, 3). [score:1]
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[+] score: 1
P1-LC) 8-mer 1st hsa-miR-650 ING4 20381459 rs77080081 15: 40382144 A G. [score:1]
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