miR-101 inhibits autophagy and enhances cisplatin-induced apoptosis in hepatocellular carcinoma cells
miR-101 inhibits autophagy and enhances cisplatin-induced apoptosis in hepatocellular carcinoma cells
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miR-101抑制自噬并增强顺铂诱导的肝癌细胞凋亡
DOI：
10.3892/or.2013.2338
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发表时间：
2013-05-01
期刊：
影响因子：
4.2
通讯作者：
Li, Xiangcheng
中科院分区：
文献类型：
--
作者：
Xu, Yonghua;An, Yong;Li, Xiangcheng
肝细胞癌（HCC）由于诊断晚和治疗选择差，在癌症相关死亡率中排名第三。自噬是溶酶体介导的蛋白质和细胞器降解过程，其特征在于形成双膜囊泡，称为自噬体。越来越多的证据表明，自噬是肝癌细胞抵抗药物诱导凋亡的一种生存机制。在这项研究中，我们发现自噬在肝癌细胞系HepG 2中被miR-101抑制。miR-101通过包括RAB 5A、STMN 1和ATG 4D在内的靶点抑制自噬。此外，miR-101增强顺铂诱导的HepG 2细胞系的凋亡。可能的机制。这种作用可能是通过抑制自噬。我们的研究结果表明，miR-101和自噬在肝癌顺铂化疗耐药性中发挥着新的关键作用。我们建议，靶向miR-101/自噬的基因治疗应进一步研究作为一个潜在的替代治疗策略HCC。
Hepatocellular carcinoma (HCC) ranks third in cancer-related mortality due to late diagnosis and poor treatment options. Autophagy is a lysosome-mediated protein and organelle degradation process which is characterized by the formation of double-membrane vesicles, known as autophagosomes. Increasing evidence reveals that autophagy functions as a survival mechanism in liver cancer cells against drug-induced apoptosis. In this study, we found that autophagy was suppressed by miR-101 in the HCC cell line HepG2. miR-101 inhibited autophagy via targets including RAB5A, STMN1 and ATG4D. Moreover, miR-101 enhanced apoptosis induced by cisplatin in the HepG2 cell line. The possible mechanism. of this effect may be through inhibition of autophagy. Our results indicate a novel and critical role for miR-101 and autophagy in the chemoresistance of cisplatin in HCC. We propose that gene therapy targeting miR-101/autophagy should be investigated further as a potential alternative therapeutic strategy for HCC.