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Ribe successful miR-634 detection in RT-PCR assays [43?5]. An explanation for the discrepancy between studies could be that miR-634 is modified under certain cell-type specific conditions. Of note, modifications at the 3' end are not uncommon for microRNAs [46, 47] and may prevent miR-634 detection by RT-PCR. Therefore, in order to monitor miR-634 levels in tumors, a specific high throughput miR-6
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F this pathway is responsible for the effect of miR-634 on cisplatin resistance. In the future, therapeutic delivery of this miRNA to drugThe ovarian carcinoma cell line A2780, colon carcinoma cell line HCT8, bladder carcinoma cell line T24 and their cisplatin-resistant derivatives A2870 DDP, HCT8 DDP, and T24 DDP10 have been described before [14, 15, 48, 49]. Resistant cell lines were routinely c
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Ightly controlled. In addition, it may be advantageous for cells to switch off production of proteins for signaling pathways that are not active. Repression of oncogene activity often leads to cell death in cancer cells, a phenomenon known as `oncogene addiction' [30]. The reduction in cell viability observed in the ovarian cancer cell lines upon overexpression of miR-634 may be caused by repressi
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Ightly controlled. In addition, it may be advantageous for cells to switch off production of proteins for signaling pathways that are not active. Repression of oncogene activity often leads to cell death in cancer cells, a phenomenon known as `oncogene addiction' [30]. The reduction in cell viability observed in the ovarian cancer cell lines upon overexpression of miR-634 may be caused by repressi
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In Kinase C ), and is only conserved in primates. miR-634 has been first detected in colon cancer cells [21] via miRNA serial analysis of gene expression (miRAGE). Afterwards, miR-634 has been identified as a miRNA able to regulate the expression of the androgen receptor (AR) in prostate cancer cells [22]. Repression of AR resulted in a reduced viability, however, the effect of miR-634 overexpress
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In Kinase C ), and is only conserved in primates. miR-634 has been first detected in colon cancer cells [21] via miRNA serial analysis of gene expression (miRAGE). Afterwards, miR-634 has been identified as a miRNA able to regulate the expression of the androgen receptor (AR) in prostate cancer cells [22]. Repression of AR resulted in a reduced viability, however, the effect of miR-634 overexpress
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This set of 23 expressing tumors this relation was not significant. It is possible that in a larger dataset this relation becomes significant. We did not observe an inverse relation between miR-634 and CCND1 expression in this dataset. Altogether, our findings show that overexpression of miR-634 leads to direct repression of RSK2, CCND1, GRB2 and ERK2 in ovarian cancer cell lines and ovarian cance
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Ribe successful miR-634 detection in RT-PCR assays [43?5]. An explanation for the discrepancy between studies could be that miR-634 is modified under certain cell-type specific conditions. Of note, modifications at the 3' end are not uncommon for microRNAs [46, 47] and may prevent miR-634 detection by RT-PCR. Therefore, in order to monitor miR-634 levels in tumors, a specific high throughput miR-6
1
Cer [8]. The observation that miR-634 is able to regulate multiple Ras-MAPK pathway genes instead of one key mediator is thought-provoking. Interestingly, many miRNAs appear to synergistically regulate a set of genes that participate in similar processes, such as the miR-17-cluster (regulates genes involved in growth control) [23], let-7 (represses Ras and its downstream target HMGA2) [24, 25] and
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Cer [8]. The observation that miR-634 is able to regulate multiple Ras-MAPK pathway genes instead of one key mediator is thought-provoking. Interestingly, many miRNAs appear to synergistically regulate a set of genes that participate in similar processes, such as the miR-17-cluster (regulates genes involved in growth control) [23], let-7 (represses Ras and its downstream target HMGA2) [24, 25] and