miR-101 inhibits autophagy and enhances cisplatin-induced apoptosis in hepatocellular carcinoma cells

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...

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Veröffentlicht in:Oncology reports 2013-05, Vol.29 (5), p.2019-2024
Hauptverfasser: XU, YONGHUA, AN, YONG, WANG, YUN, ZHANG, CHANGHE, ZHANG, HAI, HUANG, CHANGJUN, JIANG, HAO, WANG, XUEHAO, LI, XIANGCHENG
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Sprache:eng
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Zusammenfassung: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.
ISSN:1021-335X
1791-2431
DOI:10.3892/or.2013.2338