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20 publications mentioning hsa-mir-1247

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-1247. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 267
Interestingly, RCC2 showed significant transcriptional downregulation due to expression of mimic miR-1247 in MIA PaCa-2, PANC-1, and SUIT-2 cells, whereas RCC2 mRNA expression was slightly decreased in AsPC-1 and CFPAC-1 cell lines (Supplementary Figure 1). [score:8]
Here, we found that miR-1247 is frequently downregulated in pancreatic cancer cells compared with normal pancreatic tissue and its expression is restored by 5-aza-dC treatment, suggesting that abnormal expression of miR-1247 is epigenetically regulated due to DNA hypermethylation in pancreatic cancer cells. [score:8]
We previously identified several putative target genes of miR-1247 by target prediction algorithm “TargetScan” in colorectal cancer [17]. [score:7]
Further functional analyses of miR-1247 revealed that it directly represses the regulator of chromosome condensation 2 (RCC2) by targeting 3′untranslating region. [score:7]
RCC2 is a target of miR-1247 in pancreatic cancer cellsWe next focused on the mechanism underlying the tumor suppressor function of miR-1247 in association with its target genes. [score:7]
Notably, restoration of miR-1247 clearly inhibited pancreatic tumorigenesis and suppressed tumor growth in vivo, strengthening our conclusion that miR-1247 functions as a tumor suppressor in pancreatic cancer. [score:7]
We provided in this study as first evidence that epigenetically downregulated miR-1247 could play a role as tumor suppressor in pancreatic cancer. [score:6]
In addition, expression and methylation profiles in pancreatic cancer obtained from TCGA database showed significant inverse correlation which supporting that expression of miR-1247 is regulated by CpG island hypermethylation. [score:6]
Based on expression analysis of miR-1247 in pancreatic cancer cell lines treated with 5-aza-dC, we strongly suspected that DNA methylation was one of the regulatory mechanisms of miR-1247 expression. [score:6]
We conclude that overexpression of miR-1247 is responsible for decreasing RCC2 levels by targeting 3′UTR in pancreatic cancer. [score:5]
Functional analysis suggested that miR-1247 suppresses pancreatic tumorigenesis by targeting RCC2 both in vitro and in vivo. [score:5]
Overexpression of miR-1247 in pancreatic cancer cells inhibits cell growth and proliferation in vitro and in vivo. [score:5]
Our functional analyses described that miR-1247 mimic treated pancreatic cancer cells showed strong inhibitory properties of miR-1247 in cell growth, migration, and invasion, demonstrating that miR-1247 acted as a tumor suppressor in vitro. [score:5]
These results indicate that miR-1247 is able to regulate the expression of RCC2 by directly binding to its 3′UTR. [score:5]
We next focused on the mechanism underlying the tumor suppressor function of miR-1247 in association with its target genes. [score:5]
We found that pancreatic cancer cells expressing ectopic miR-1247 suppress cell migration and invasion. [score:5]
Considering the basal expression level and re -expression level after 5-aza-dC, we suspect that CpG islands in the promoter region of miR-1247 are hypermethylated in pancreatic cancer cells. [score:5]
Interestingly, we observed significant inhibition of migration (ranging from 42% to 70%) and invasion (ranging from 70% to 87%) with miR-1247 expression in all pancreatic cancer cell lines we tested (Figure 5A, 5B). [score:5]
Both primary and mature miR-1247 are indeed transcriptionally downregulated in most pancreatic cancer cell lines compared to expression level of normal tissue (< 5-fold) (Figure 1A, 1B). [score:5]
Based on in vitro data showing significant growth inhibition in cells expressing ectopic miR-1247, we investigated whether miR-1247 could suppress pancreatic cancer tumorigenicity in vivo. [score:5]
We found that 72 h after transfection, ectopic expression of miR-1247 suppressed pancreatic cancer cell growth (Figure 4A). [score:5]
We wondered whether its transcriptional downregulation of miR-1247 is under epigenetic control, and so we treated the demethylating agent 5-aza-2′-deoxycytidine (5-aza-dC) to five pancreatic cancer cell lines (AsPC-1, CFPAC-1, MIA PaCa-2, PANC-1, and SUIT-2) and performed qRT-PCR analysis of both pri-miR-1247 and mature miR-1247. [score:4]
Previous report had been demonstrated that miR-1247 is regulated by DNA hypermethylation in colon cancer using both gene expression and genome-wide methylation profiles [16]. [score:4]
Our results provide that miR-1247 is epigenetically regulated by hypermethylation and may function as a tumor suppressor in pancreatic cancer. [score:4]
To determine whether epigenetically regulated miR-1247 has tumor-suppressive properties in pancreatic cancer cells, we transfected five pancreatic cancer cell lines with miRNA mimics of miR-1247 and non-coding negative controls. [score:4]
Figure 4Overexpression of miR-1247 in pancreatic cancer cells inhibits cell growth and proliferation in vitro and in vivo(A) Growth curves and (B) MTT assays of pancreatic cancer cells (AsPC-1, CFPAC-1, MIA PaCa-2, PANC-1, and SUIT-2) transfected with non-coding negative control (AllStar Neg. ) [score:4]
The data showed that overexpression of miR-1247 mimics decreased RCC2 expression in the tumor tissues compared to control tissues (Figure 6E). [score:4]
In summary, our results indicate that aberrant expression of miR-1247 is regulated by DNA hypermethylation in pancreatic cancer. [score:4]
However, the functions, target genes, as well as the regulatory mechanism of miR-1247 are still unknown in pancreatic cancer. [score:4]
We observed significantly increased expression of pri-miR-1247 after 5-aza-dC treatment in most pancreatic cancer cell lines, but not in CFPAC-1 cells (Figure 1C). [score:3]
Functional effects of miR-1247 overexpression in pancreatic cancer cells. [score:3]
Investigation of methylation and transcriptional expression in the large TCGA dataset revealed that methylation and transcriptional expression of miR-1247 were inversely correlated (correlation coefficient = −0.21, p = 0.004) (Figure 3A). [score:3]
MIA PaCa-2 and PANC-1 cells were transfected with miR-1247 mimics or non -targeting negative controls for 48 h. Cells (1 × 10 [6]) were then injected subcutaneously into the right flanks of 6 week old female nude mice. [score:3]
Therefore, we wonder whether methylation of miR-1247 is correlated with its expression in pancreatic tumors by analyzing data set of pancreatic cancer samples (n = 177) from the Cancer Genome Atlas (TCGA). [score:3]
Correlation between expression levels and methylation beta-values of miR-1247 in pancreatic primary tissue samples. [score:3]
In agreement with these results, RCC2 mRNA and protein levels were also significantly decreased in the pancreatic cancer cell lines overexpressing miR-1247 (Figure 6C, 6D). [score:3]
When miR-1247 was cotransfected, the relative luciferase activity of the reporter containing RCC2 wt-3′UTR was significantly suppressed ranging from 15% to 60% in comparison to AllStar negative control (Figure 6B). [score:3]
Figure 1(A– B) (qRT-PCR) analysis of expression pattern of pri-miR-1247 and mature miR-1247 in pancreatic cancer cell lines (AsPC-1, CFPAC-1, MIA PaCa-2, PANC-1, and SUIT-2) and normal pancreatic tissue (NP). [score:3]
We also determined that ectopic expression of miR-1247 resulted in robust reduction of cell proliferation, migration, and invasion. [score:3]
In order to confirm the DNA methylation associated with abnormal expression of miR-1247, bisulfite sequencing analysis was performed to assess the methylation status of CpG islands of miR-1247, and we observed that miR-1247 is hypermethylated in five pancreatic cancer cell lines. [score:3]
MIA PaCa-2 and PANC-1 cells (1 × 10 [6]) were transfected with miR-1247 mimics or non -targeting negative control according to the manufacturer's protocols, screened for stability, and then subcutaneously injected into the flank region. [score:3]
Overall, all of these data suggest that miR-1247 might play a role as tumor suppressor in pancreatic cancer. [score:3]
The luciferase activity assay with a reporter containing the miR-1247 binding sequence at the 3′ UTR of RCC2 mRNA suggested that miR-1247 directly targets the 3′ UTR of RCC2 mRNA. [score:3]
After 5 weeks, the tumors were harvested and it was noteworthy that tumors formed in the miR-1247 group were much smaller than those in the group transfected with non -targeting negative control (Figure 4C). [score:3]
Analysis of miR-1247 expression in pancreatic cancer cell lines. [score:3]
RCC2 is a target of miR-1247 in pancreatic cancer cells. [score:3]
Pearson's correlation coefficient was used to determine the correlation between the methylation level (beta value) of miR-1247 locus and the expression level (RPM, reads per million) of miR-1247 in 177 tumor samples. [score:3]
These data suggest that ectopic expression of miR-1247 significantly decreased growth and metabolism of pancreatic cancer cell lines. [score:3]
Overall, these results strongly suggest that miR-1247 has tumor suppressor functions in pancreatic cancer cells both in vitro and in vivo. [score:3]
MiR-1247 was first identified in colorectal cancer and reported to be downregulated in colorectal and gastric cancers [16, 17]. [score:3]
This suppression of cell growth by miR-1247 was confirmed in a xenograft mo del. [score:3]
Figure 3(A) Pearson's correlation coefficient was used to determine the correlation between the methylation level (beta value; x axis) of miR-1247 locus and the expression level (RPM, reads per million; y axis) of miR-1247 in 177 tumor samples. [score:3]
Correlation between methylation and transcriptional expression of miR-1247 in pancreatic cancer cells and primary tumors. [score:3]
MiR-1247 showed dense DNA methylation in pancreatic cancer cells and demethylation (76%–100%) was observed in cells upon 5-aza-dC treatment, strongly supporting idea that the re -expression of silenced miR-1247 by 5-aza-dC was leading to DNA demethylation (Figure 2). [score:3]
In our study, we showed that miR-1247 reduced the expression level of RCC2 at both mRNA and protein levels in pancreatic cancer cells. [score:3]
Furthermore, we performed migration and invasion assays to analyze the effect of miR-1247 expression on pancreatic cancer cell migration and invasion. [score:2]
qRT-PCR was performed on a C1000 Thermal Cycler (BioRad) using the PCR primers listed in Supplementary Table 1. To ectopically express miR-1247 in pancreatic cancer cell lines, cells were transfected with 20 nM hsa-miR-1247 miScript mimic (MSY0005899, Qiagen), or Allstars Negative Control siRNA (1027281, Qiagen) using Lipofectamine 2000 (Invitrogen) following the manufacturer's instructions. [score:2]
To investigate whether miR-1247 might be regulated by DNA hypermethylation in pancreatic cancer, we first analyzed the expression of miR-1247 in five pancreatic cancer cell lines and normal pancreatic tissue using quantitative RT-PCR (qRT-PCR). [score:2]
MiR-1247 targets RCC2 in pancreatic cancer cells. [score:2]
Correspondingly, CpG islands hypermethylation of miR-1247 was also observed in pancreatic tumor specimens, supporting the idea that epigenetic silencing of miR-1247 is truly regulated by CpG island hypermethylation. [score:2]
MiR-1247 suppressed in vivo tumor growth. [score:2]
Therefore we examined whether miR-1247 is able to interact directly with the 3′UTR of RCC2. [score:2]
Pancreatic cancer cells were co -transfected with wt RCC2 or non -targeting negative control, and miR-1247 mimics together with Renilla psiCHECK2 vector for 48 h. Relative firefly/ Renilla luciferase activity was then quantified using a Dual-Luciferase Reporter Assay (Promega) according to the manufacturer's protocol. [score:2]
Quantitative methylation-specific PCR (qMSP) analysis was performed to assess the methylation pattern of CpG islands upstream of miR-1247 gene locus in pancreatic cancer cell lines and in 5-aza-dC treated cells. [score:1]
Figure 2(A) Quantitative methylation-specific PCR (qMSP) analysis of methylation level of miR-1247 in pancreatic cancer cell lines. [score:1]
Using a promoter–activity-prediction program, we found putative binding sites of miR-1247 in the 3′ UTR of RCC2 (Figure 6A). [score:1]
The miR-1247 binding sequence at the 3′UTR of RCC2 mRNA (wt) was cloned downstream of the firefly luciferase reporter gene, and then cotransfected with mimic miR-1247 or AllStar negative control into the pancreatic cancer cell lines. [score:1]
To confirm this, we assessed DNA methylation level in the proximal region of miR-1247 by bisulfite sequencing analysis (Figure 2B). [score:1]
In agreement with the cell growth curve, the volumes of tumors treated with miR-1247 mimics were significantly smaller than tumors injected with non-coding negative control. [score:1]
We therefore asked whether DNA methylation in the promoter region of miR-1247 is responsible for the transcriptional silencing of miR-1247 in pancreatic cancer cells. [score:1]
or miR-1247 mimics. [score:1]
We therefore screened 13 genes (BLCAP, BRSK1, CPEB4, CREBZF, IGSF9B, MOCS1, MYCBP2, PHF21A, RARA, RBM19, RCC2, STX1B, and ZBTB46) in five pancreatic cancer cell lines to determine whether miR-1247 induce transcriptional changes of candidate genes (Supplementary Figure 1). [score:1]
Figure 6(A) Schematic diagram of RCC2 3′ UTR region indicating putative miR-1247 binding sites. [score:1]
In the present study, we found that CpG island in the upstream region of miR-1247 gene was frequently hypermethylated correlated with transcriptional silencing of miR-1247 in pancreatic cancer cell lines and primary tumors. [score:1]
These data suggest that hypermethylation in the proximal region of miR-1247 has a cancer specific manner correlated with aberrant transcriptional silencing of miR-1247 in primary pancreatic tumors. [score:1]
Functional analyses of miR-1247 in pancreatic cancer cells. [score:1]
On the other hand, miR-1247 mimic transfected cells migrated into the wound at a much slower rate in most pancreatic cancer cells (Figure 5C). [score:1]
We confirmed that mature miR-1247 was re-expressed after treatment with 5-aza-dC, consistent with studies in most other pancreatic cancer cell lines (however, not in AsPC-1 cells) that measured primary transcript of miR-1247. [score:1]
Therefore, we concluded that miR-1247 is definitely epigenetically silenced in pancreatic cancer cells. [score:1]
We then hypothesized that miR-1247 may be frequently hypermethylated in pancreatic cancer, as in the examples above, with significant biological roles associated with tumorigenesis. [score:1]
Methylation analyses of miR-1247 in pancreatic cancer cell lines. [score:1]
Bisulfite sequence analysis was carried out for miR-1247 in AsPC-1, CFPAC-1, MIA PaCa-2, PANC-1, and SUIT-2 cells. [score:1]
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[+] score: 77
We postulated that down-regulation of these predicted targets by ectopic expression of miR-941 and miR-1247 would negatively impact cell migration. [score:8]
Ectopic expression of miR-1247 significantly reduced cancer cell proliferation and migration in HCT116 and DLD1 cells, suggesting that miR-1247 may function as a tumor suppressor. [score:5]
To verify that the up-regulation of these miRNAs was consequent to DNA demethylation after 5-aza-dC treatment, we assessed changes in DNA methylation status in the proximal regions of miR-941-1/3, miR-1237 and miR-1247 by bisulfite genomic sequencing (Figure 2). [score:4]
Over -expression of miR-941, miR-1237, and miR-1247 in HCT116, D KO, and DLD1 cells was achieved by transfecting the cells with 20 nM miRNA duplexes that mimicked the mature miR-941 (MSY0004984, Qiagen), miR-1237 (MSY0005592, Qiagen), and miR-1247 (MSY0005899, Qiagen). [score:3]
For example, ADAM metallopeptidase domain 15 (ADAM15) is a predicted target of miR-1247 and encodes a transmembrane glycoprotein important for cell adhesion [27]. [score:3]
Finally, the transmembrane glycoprotein, ADAM15, might also be targeted by miR-1247, to facilitate prostate cancer metastasis [35]. [score:3]
To determine if expression of these epigenetically silenced miRNAs would affect cancer cell growth and migration, we transfected HCT116 cells with miRNA mimics of miR-941 (the mature form of miR-941-1 and -3), miR-1237, miR-1247, and a non-coding negative control (AllStars Neg. [score:3]
Interestingly, in D KO cells, where miR-1247 is demethylated and expressed at higher levels than HCT116 cells, additional exposure to miR-1247 mimics did not result in decreases of cell growth but caused impaired migration. [score:3]
These observations are consistent with the functions of several predicted targets of miR-1247 (http://www. [score:3]
Conversely, in D KO cells, where miR-1247 is already demethylated and re-expressed, transfection with additional miR-1247 mimics did not have any effects on cell growth and metabolism (Figure S5A and B). [score:3]
Finally, similar suppressive effects on cell migration were independently observed in DLD1 cells (Figure S4C) and D KO cells (Figure S5C) transfected with miR-941 and miR-1247 mimics. [score:3]
These observations suggested that miR-1247 may be tumor-suppressive in colon cancer and its epigenetic silencing is therefore beneficial for cancer growth. [score:3]
Another potential target for miR-1247 is FosB, which dimerizes with Jun protein to activate transcription of proteases involved in tumor migration and invasion [34]. [score:3]
Furthermore, computationally predicted targets of miR-941 and miR-1247 included several genes involved in cell migration and invasion. [score:3]
The discrepancies between the phenotypes of ectopic miR-1247 expression in HCT116, DLD1, and D KO cells may reflect the different concentrations at which distinct cellular functions are modulated by miR-1247. [score:3]
Alternatively, it may be due to the presence of different targets for miR-1247 in HCT116 and D KO cells. [score:3]
Hence, we tested the effects of ectopic expression of miR-941, miR-1237, and miR-1247 on cell mobility in HCT116 cells. [score:3]
miR-941 and miR-1247 suppress cell growth and migration in colon cancer cells. [score:3]
We focused on two important aspects of cancer development, growth and migration, and selected miR-941, miR-1237, and miR-1247 for functional studies. [score:2]
miR-1247, miR-1826, and miR-219-2 are located in intergenic regions and therefore, are unlikely to be co-regulated by a host gene promoter. [score:2]
We observed a similar decrease in cell proliferation and metabolic function in DLD1 colon cancer cells transfected with miR-1247 mimic (Figure S4A and B). [score:1]
), miR-941, or miR-1247 mimics. [score:1]
), miR-941, or miR-1247. [score:1]
0020628.g002 Figure 2Bisulfite sequencing was carried out for (A) miR-941, (B) miR-1237, and (C) miR-1247 in parental HCT116 cells, HCT116 cells treated with 5 µM 5-aza-dC for 48 hr, and D KO cells. [score:1]
Taken together, these observations suggest that the epigenetic silencing of miR-941 and miR-1247 may facilitate colon cancer cell migration and invasion. [score:1]
HCT116 cells transfected with miR-941 and miR-1247 mimics and the AllStars Negative Control were re-plated on coverslips at 24 hr post-transfection. [score:1]
Functional analysis of miR-941, miR-1237, and miR-1247 in HCT116 cells. [score:1]
Figure S4 Functional analysis of miR-941, miR-1237, and miR-1247 in DLD1 cells. [score:1]
was carried out for (A) miR-941, (B) miR-1237, and (C) miR-1247 in parental HCT116 cells, HCT116 cells treated with 5 µM 5-aza-dC for 48 hr, and D KO cells. [score:1]
), miR-941, miR-1237, or miR-1247 mimics. [score:1]
Figure S5 Functional analysis of miR-941 and miR-1247 in D KO cells. [score:1]
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[+] score: 42
1004188.g001 Figure 1 miR-10b-5p, miR-1247-5p, miR-196a-5p, miR-196b-5p, and miR-615-3p were identified as differentially expressed in Huntington's disease prefrontal cortex compared to non-neurological disease controls by Illumina miRNA-sequencing. [score:6]
Five of these, miR-10b-5p, miR-196a-5p, miR-196b-5p, miR-615-3p and miR-1247-5p, were up-regulated in HD at genome-wide significance (FDR q-value<0.05), and three of these five, miR-196a-5p, miR-196b-5p and miR-615-3p, were expressed at near zero levels in the control brains. [score:6]
miR-10b-5p, miR-1247-5p, miR-196a-5p, miR-196b-5p, and miR-615-3p were identified as differentially expressed in Huntington's disease prefrontal cortex compared to non-neurological disease controls by Illumina miRNA-sequencing. [score:6]
22 differential expressed targets of miR-10b-5p, miR-196a, miR-196b, miR-1247 and miR-615-3p. [score:5]
miRWalk targets of miR-196a, miR-196b and miR-1247 were not strand specific. [score:3]
Since miR-1247 had just two validated targets, it was removed from analysis. [score:3]
miR-1247-5p was expressed at moderate levels in both control (mean = 49.44) and HD brain (mean = 102.01). [score:3]
Seed sequences differ for miR-10b-5p (ACCCUGU), miR-615-3p (CCGAGCC) and miR-1247-5p (CCCGUCC) suggesting these miRNA have different targets, while miR-196a-5p and miR-196b-5p share a seed sequence (AGGUAGU) and only differ by a single base difference in mature miRNA sequence. [score:3]
The miRWalk database contained 84 unique targets for miR-10b-5p, 80 for miR-196a, 40 for miR-196b, two for miR-1247 and twelve for miR-615-3p. [score:3]
miR-1247-5p showed association with later age at death (β = −0.013, p-value = 0.024) in controls. [score:1]
No association to any clinical features was seen for miR-1247-5p. [score:1]
miR-1247-5p was not significantly correlated with these miRNAs (Spearman r range 0.13–0.51; p range 0.09–0.70). [score:1]
According to the miRNA search program “PubmiR,” [37] miR-196b-5p, miR-1247-5p and miR-615-3p have not been previously reported in HD miRNA studies. [score:1]
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[+] score: 20
According to the result, we found that although the population -based effects and inherent differences inevitably emerged as the previous report [33], the tendency of the expression patterns was consistent with the NGS findings, as miR-107 and miR-223-3p showed the upregulated expression levels in cancerous penile tissues, while miR-1247-5p and miR-509-3p showed the downregulated expression levels in cancerous penile tissues, which again verified the smRNA-seq sequencing data (S6 Fig). [score:13]
As expected, most majority of the miRNAs, either upregulated in the cancer tissues, such as miR-223-3p [61], miR-421 [62], miR-424-5p [63], miR-1260b [64] etc, or downregulated in the penile cancer, such as miR-205-5p [65], miR-211-5p [65– 66], miR-365-3p [67] and miR-1247 [68] etc, were entitled the similar roles in carcinogenesis of bladder cancer, retinoblastoma, breast cancer, nasopharyngeal cancer, pancreatic cancer and several other cancer types [61– 68]. [score:7]
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[+] score: 8
Among the top differentially expressed miRNAs, miR-183 and miR-182 are most up-regulated in cancer samples (highest fold change) while miR-1247 and miR-199b-5p were most down-regulated in cancer samples compared to normal samples (Table  1). [score:8]
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[+] score: 8
Our analysis confirms the upregulation of miR-10b-5p, miR-196a-5p, miR-196b-5p, miR-615-3p and miR-1247-5p in HD. [score:4]
Hoss and colleagues [9] related five upregulated miRNAs (miR-10b-5p, miR-196a-5p, miR-196b-5p, miR-615-3p and miR-1247-5p) located in the HOX gene cluster to HD pathogenesis. [score:4]
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[+] score: 6
Other miRNAs from this paper: hsa-mir-486-1, hsa-mir-486-2
They found that miR-1247, which is predicted to target CIT (http://www. [score:3]
Therefore, the lack of miR-1247 may result in increased CIT expression in colon cancer tissues. [score:3]
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8
[+] score: 6
Other miRNAs from this paper: hsa-mir-4285, hsa-mir-3648-1, hsa-mir-3648-2
PCNXL3 was reported to be one of the top 20 genes with the highest correlations with colon adenocarcinoma [42], MIR4285 and MIR3648 were shown to be differentially expressed in colon adenomas [43, 44], and MiR1247 as a potential tumor suppressive gene [45]. [score:5]
Table 3 lists the top 10 most significant hyper-methylated DMRs (distance to transcription start site [TSS] were from -1,000 to +1,000 base-pair [bp] DNA) for Cancer/control pair, and the annotated genes are PCNXL3, MIR4285, NLGN2, MIR3648, HOXA4, CLDN23, TONSL, GNAS, TUBB8 and MIR1247. [score:1]
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[+] score: 5
Moreover, miR-1247 was detected to work as a potential tumor suppressor by targeting MAP3K9 in progression of osteosarcoma [7]. [score:5]
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[+] score: 5
Shi S. Lu Y. Qin Y. Li W. Cheng H. Xu Y. Xu J. Long J. Liu L. Liu C. miR-1247 is correlated with prognosis of pancreatic cancer and inhibits cell proliferation by targeting neuropilins Curr. [score:5]
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Zhao F. Lv J. Gan H. Li Y. Wang R. Zhang H. Wu Q. Chen Y. MiRNA profile of osteosarcoma with CD117 and stro-1 expression: miR-1247 functions as an onco-miRNA by targeting MAP3K9Int. [score:5]
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[+] score: 4
Other miRNAs from this paper: hsa-mir-29a, hsa-mir-101-1, hsa-mir-139, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-142, hsa-mir-144, hsa-mir-127, hsa-mir-154, hsa-mir-185, hsa-mir-195, hsa-mir-29c, hsa-mir-101-2, hsa-mir-380, hsa-mir-381, hsa-mir-323a, hsa-mir-520e, hsa-mir-520a, hsa-mir-518c, hsa-mir-520d, hsa-mir-518a-1, hsa-mir-518d, hsa-mir-518a-2, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-509-1, hsa-mir-576, hsa-mir-548a-1, hsa-mir-586, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-599, hsa-mir-548a-3, hsa-mir-607, hsa-mir-613, hsa-mir-548c, hsa-mir-625, hsa-mir-634, hsa-mir-642a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-656, hsa-mir-509-2, hsa-mir-509-3, hsa-mir-1208, hsa-mir-548e, hsa-mir-548j, hsa-mir-1290, 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-1324, hsa-mir-1825, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-323b, hsa-mir-548w, hsa-mir-548x, hsa-mir-548y, hsa-mir-642b, 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
Indeed, although CTNNA2 can be regulated by primate-specific miRNAs common to both monkeys and humans (miR-513a-3p, miR-518a-5p, miR-548a-5p, miR-576-5p, miR-586, miR-607, miR-625, miR-642), a number of miRNAs present in Homo sapiens but not in Macaca mulatta (miR-1208, miR-1247, miR-1290, miR-1324, miR-1825, miR-613 and miR-634) also target CTNNA2 [19], [29]. [score:4]
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[+] score: 3
Besides, the newly detected 3p arms of hsa-mir-511-1, hsa-mir-511-2, hsa-mir-1273c and hsa-mir-1247 also have higher expression levels than the originally annotated 5p arm. [score:3]
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[+] score: 3
Comparison between the non-recurrent and recurrent sub-group revealed significant expression differences of 9 miRNAs, miR-138-1-5p, miR-181-2-5p, miR-181-5p, miR-182-5p, miR-29b1-3p, miR-29b2-3p, miR193b-3p, miR-15a-3p and miR-1247-5p, five of which also discriminated between non-recurrent and metastatic sub-group. [score:3]
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15
[+] score: 3
Other miRNAs from this paper: hsa-mir-129-1, hsa-mir-129-2
For example, methylation -induced miR-1247 silencing promotes cancer cell invasion and migration in non-small cell lung cancer [42], while miR-129-5P methylation was associated with expression of human valosin-containing protein in osteosarcoma [43]. [score:3]
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16
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Other miRNAs from this paper: hsa-mir-205, hsa-mir-210, hsa-mir-492
In pancreatic juice, increased levels of miR-205, miR-210, miR-492, and miR-1247 are associated with poor prognosis for pancreatic adenocarcinoma [30]. [score:1]
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Similarly, the rs2288947 A>G polymorphism may cause miRNA–lncRNA gain by binding hsa-miR-665 or hsa-miR-6840-3p, and miRNA–lncRNA loss by binding hsa-miR-1247-3p. [score:1]
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In addition, Yan et al. (2011) performed a genome-wide methylome analysis entailing deep sequencing of MBD (methylated DNA binding domain)-isolated DNA in HCT116 cells, and identified a number of methylated genes, including miR-941, miR-1237, and miR-1247. [score:1]
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In this study, we used time-lapse video microscopy to observe cell movement in the scratch-wound assay, validated the results using the transwell migration assay, and identified the migration-suppressing miRNA (miR-134) and migration-facilitating miRNAs (miR-1247, miR-1244, miR-146b-3p, miR-1471, miR-188-3p, miR-661, miR-891a, miR-891b and miR-767-5P) in SK-HEP-1 cells. [score:1]
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We also choose to include seven miRNAs (mir-370, mir-337-5p, mir-376c, mir-377, mir-1247, mir-758 and mir-300) that are located on the q arm of chromosome 14, which has been found to be aberrant and implicated in many types of cancer [24]. [score:1]
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