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MicroRNA-374a Promotes Hepatocellular Carcinoma Cell Proliferation by Targeting Mitogen-Inducible Gene 6 (MIG-6)

机译:MicroRNA-374A通过靶向丝介质诱导基因6(MIG-6)促进肝细胞癌细胞增殖

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摘要

Hepatocellular carcinoma (HCC) is a disease with poor prognosis rates and ineffective therapeutic options. Previous studies have reported the involvement of mitogen-inducible gene 6 (MIG-6) as a negative regulator in tumor formation. MicroRNAs (miRNAs) play crucial roles in the development of different types of cancer. However, the underlying mechanisms of miRNAs in HCC are poorly understood. This study was aimed to investigate the role of miR-374a in HCC and its role in the regulation of expression of MIG-6. The results showed that MIG-6 overexpression significantly inhibited cell viability of HepG2 cells after 4 days post-transfection. Moreover, MIG-6 was a direct target of miR-374a, and the expression of MIG-6 was remarkably downregulated by the overexpression of mi R-374a in HepG2 cells. Furthermore, we found that overexpression of miR-374a promoted cell viability; however, the protective effect was abolished by MIG-6 overexpression. In addition, overexpression of miR-374a activated the EGFR and AKT/ERK signaling pathways by regulation of MIG-6. Our findings suggest that miR-374a could promote cell viability by targeting MIG-6 and activating the EGFR and AKT/ERK signaling pathways. These data provide a promising therapeutic strategy for HCC treatment.
机译:肝细胞癌(HCC)是一种患有差,预后率差和无效治疗选择。以前的研究报告介导诱导型诱导基因6(MIG-6)作为肿瘤形成中的负调节剂。 MicroRNA(miRNA)在不同类型的癌症的发展中起着至关重要的作用。然而,HCC中MIRNA的潜在机制尚不清楚。本研究旨在探讨miR-374a在HCC中的作用及其在MIG-6表达调控中的作用。结果表明,在转染后4天后,MIG-6过表达显着抑制HepG2细胞的细胞活力。此外,MIG-6是miR-374a的直接靶标,通过HepG2细胞中的Mi R-374a的过表达显着下调MIG-6的表达。此外,我们发现miR-374a的过表达促进了细胞活力;然而,通过MIG-6过表达废除了保护作用。此外,MiR-374a的过表达通过调节MIG-6激活EGFR和AKT / ERK信号通路。我们的研究结果表明,MIR-374A可以通过靶向MIG-6来促进细胞活力并激活EGFR和AKT / ERK信号通路。这些数据为HCC治疗提供了有希望的治疗策略。

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