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miR-1271 enhances the sensitivity of colorectal cancer cells to cisplatin

机译:miR-1271增强大肠癌细胞对顺铂的敏感性

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摘要

The high mortality of colorectal cancer (CRC) is likely caused by early invasion and metastasis. The chemoresistance of tumor cells is the critical reason for treatment failure. The present study aimed to develop targeted solutions to overcome chemotherapy drug resistance in CRC. CCK-8 assay was used to examine SW480 cell viability. SW480 cell apoptosis was examined using flow cytometry. The present study demonstrated that the expression of miR-1271 was significantly decreased in CRC tumors and cell lines compared with control tissues. Furthermore, the expression of microRNA (miR)-1271 was increased and decreased following the transfection of miR-1271 mimics and an inhibitor, respectively. Furthermore, miR-1271 regulated mammalian target of rapamycin (mTOR) expression by directly binding to the mTOR 3′-untranslated region and the relative luciferase activity of mTOR was decreased following miR-1271 overexpression. The results of the present study indicate that miR-1271 may be a potential target for anti-CRC therapy, particularly in the sensitivity of chemotherapeutic drugs. miR-1271 may therefore enhance the sensitivity of CRC cells to chemotherapy drugs and provide a novel approach for the gene therapy of CRC.
机译:大肠癌(CRC)的高死亡率可能是由于早期侵袭和转移引起的。肿瘤细胞的化学耐药性是治疗失败的关键原因。本研究旨在开发针对性的解决方案,以克服CRC中的化疗药物耐药性。使用CCK-8测定法检查SW480细胞活力。使用流式细胞仪检查SW480细胞凋亡。本研究表明,与对照组织相比,miR-1271在CRC肿瘤和细胞系中的表达明显降低。此外,分别转染miR-1271模拟物和抑制剂后,microRNA(miR)-1271的表达增加和减少。此外,miR-1271过表达后,通过直接结合到mTOR 3'-非翻译区,miR-1271调节了哺乳动物雷帕霉素靶标(mTOR)的表达,降低了mTOR的相对荧光素酶活性。本研究结果表明,miR-1271可能是抗CRC治疗的潜在靶标,特别是在化学治疗药物的敏感性方面。因此,miR-1271可能增强CRC细胞对化疗药物的敏感性,并为CRC基因治疗提供一种新方法。

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