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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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L lines, and the fastest growing cultures (cultures 3 and 7) showed the largest reduction in cell viability upon miR-634 overexpression. We describe that miR-634 transfection results in enhanced cisplatin sensitivity. Intriguingly, this effect of miR-634 overexpression is most apparent in resistant ovarian cancer cell lines, and also occurs in tumor cells derived from ascites. The miR-634 mediated
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L lines, and the fastest growing cultures (cultures 3 and 7) showed the largest reduction in cell viability upon miR-634 overexpression. We describe that miR-634 transfection results in enhanced cisplatin sensitivity. Intriguingly, this effect of miR-634 overexpression is most apparent in resistant ovarian cancer cell lines, and also occurs in tumor cells derived from ascites. The miR-634 mediated
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F miR-634 overexpression on tumor growth and therapy response in a genetic mouse model for ovarian cancer. However, such a study is complicated by the fact that there is no high grade serous mouse model for ovarian cancer [39, 40], and miR-634 has no murine orthologue.van Jaarsveld et al. Molecular Cancer (2015) 14:Page 9 ofmiR-Ras/ERK pathwayPt/DoxCyclin DCell cycle progressionProliferationCell d
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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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Commonly downregulated in three cisplatin/sensitive cell line pairs. Overexpression of miR-634 transiently inhibited G1-S cycle progression and enhanced apoptosis of ovarian cancer cells. Furthermore, miR-634 enhanced the chemotherapy response of cisplatin-resistant ovarian cancer cell lines and drug resistant patient-derived primary tumor cells. In addition, we observed that miR-634 overexpressio
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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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Nal file 1: Figure S11A). In addition, Ras-MAPK signaling may contribute to cisplatin resistance [19]. Our previous work has demonstrated that RSK2 depletion enhances cisplatin sensitivity [20]. Concurringly, PD0325901 augmented cisplatin toxicity at 24H after treatment (Additional file 1: Figure S11B).Discussion The aim of this study was to discover miRNAs that affect the response of ovarian canc
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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