miR-1299 suppresses cell proliferation of hepatocellular carcinoma (HCC) by targeting CDK6
作者
Zhu, HQ;Wang, GC;Zhou, X;Song, X;Gao, HJ;Ma, CQ;Chang, H;Li, HG;Liu, FF;Lu, J;Ma, JB
作者单位
[Zhu, Huaqiang; Zhou, Xu; Song, Xie; Gao, Hengjun; Ma, Chaoqun; Chang, Hong; Li, Hongguang; Liu, Fang-Feng; Lu, Jun] Shandong Univ, Shandong Prov Hosp, Dept Hepatobiliary Surg, Jinan 250014, Shandong, Peoples R China.;-;[Wang, Guangchuan] Shandong Univ, Shandong Prov Hosp, Dept Gastroenterol, Jinan 250014, Shandong, Peoples R China.;-;[Ma, Jinben] Shandong Univ, Shandong Prov Hosp, Dept Anesthesiol, 9677 Jingshi Rd, Jinan 250014, Shandong, Peoples R China.
摘要
microRNA (miRNA) plays critical role in HCC initiation and development, many miRNAs have been reported to regulate HCC progression. In this study, we studied the role of miR-1299 in cell proliferation of HCC. We found miR-1299 was significantly downregulated in HCC cells and tissues. miR-1299 overexpression inhibited cell proliferation and arrested cell cycle in G0/G1 phase analyzed by MTT assay, soft agar assay, BrdU cell proliferation assay and cell cycle assay, while miR-1299 knockdown promoted cell proliferation and accelerated G1/S transition. Further analysis suggested the key regulator of G1/S transition, cyclin-dependent kinase 6 (CDK6) was the target of miR-1299, miR-1299 inhibited CDK6 expression and bound to the 3'UTR of CDK6. When double knockdown of miR-1299 and CDK6 promoted cell proliferation copied the phenotype caused by miR-1299 overexpression, suggesting miR-1299 inhibits cell proliferation by targeting CDK6. In summary, our data revealed miR-1299 inhibits cell proliferation, and might be a target for HCC therapy. (C) 2016 Published by Elsevier Masson SAS.
关键词
CANCER CELLS; TRANSITION; APOPTOSIS