Oncotarget · 2017 · 26 citations · 26 references
MedicineMolecular BiologyOncologyCarcinogenesisMolecular OncologyOncogenesCancer Cell SignalingCell-cycle DysregulationHepatocellular CarcinomaLiver CancerSignal Transduction In CancerCell Cycle Arrest MechanismsCyclin D OverexpressionCyclin D RegulationCyclin RegulationG1 Cell-cycle ArrestG1 Phase ArrestHepatocellular Carcinoma PathogenesisSoft Agar Colony Formation Assays
// Yadong Wang 1, 2 , Teng Pan 3 , Haiyu Wang 1 , Li Li 1 , Jiangmin Li 1 , Ding Zhang 1 and Haiyan Yang 3 1 Department of Toxicology, Henan Center for Disease Control and Prevention, Zhengzhou 450016, China 2 Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang Medical University, Xinxiang 453003, China 3 Department of Epidemiology, School of Public Health, Zhengzhou University, Zhengzhou 450001, China Correspondence to: Yadong Wang, email: wangyd76@163.com Keywords: SIRT6, HCC cell, tumorigenicity, cell cycle Received: March 31, 2017     Accepted: June 04, 2017     Published: July 17, 2017 ABSTRACT Objective: This study aimed to explore the effects of overexpression of sirtuin 6 (SIRT6) on the tumorigenicity of hepatocellular carcinoma (HCC) cells . Methods : Stable SIRT6-overexpressed HCC cell lines were established by transfecting SIRT6 plasmid. Soft agar assay and tumor xenograft assay in nude mice were applied. Flow cytometry was employed to detect cell cycle distribution. Western blotting analysis was used to detect the expression of proteins. Results : Overexpression of SIRT6 attenuated HepG2 and HCCLM3 cells proliferation, colony formation in vitro and tumor formation in nude mice, and resulted in the G1 phase cell cycle arrest. Overexpression of SIRT6 reduced the expression of cyclin D1 and p-ERK proteins in both HepG2 and HCCLM3 cells. Conclusion : Overexpression of SIRT6 attenuates the tumorigenicity of HCC cells.
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