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SIRT6的过表达减弱了肝癌细胞的致瘤性。

Overexpression of SIRT6 attenuates the tumorigenicity of hepatocellular carcinoma cells.

作者信息

Wang Yadong, Pan Teng, Wang Haiyu, Li Li, Li Jiangmin, Zhang Ding, Yang Haiyan

机构信息

Department of Toxicology, Henan Center for Disease Control and Prevention, Zhengzhou 450016, China.

Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang Medical University, Xinxiang 453003, China.

出版信息

Oncotarget. 2017 Jul 17;8(44):76223-76230. doi: 10.18632/oncotarget.19297. eCollection 2017 Sep 29.

DOI:10.18632/oncotarget.19297
PMID:29100306
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5652700/
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 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.

摘要

目的

本研究旨在探讨沉默调节蛋白6(SIRT6)过表达对肝癌(HCC)细胞致瘤性的影响。

方法

通过转染SIRT6质粒建立稳定过表达SIRT6的肝癌细胞系。应用软琼脂试验和裸鼠肿瘤异种移植试验。采用流式细胞术检测细胞周期分布。用蛋白质印迹分析检测蛋白质表达。

结果

SIRT6过表达减弱了HepG2和HCCLM3细胞的增殖、集落形成及裸鼠体内肿瘤形成,并导致G1期细胞周期阻滞。SIRT6过表达降低了HepG2和HCCLM3细胞中细胞周期蛋白D1和p-ERK蛋白的表达。

结论

SIRT6过表达减弱了肝癌细胞的致瘤性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dcf/5652700/fb4390ac692a/oncotarget-08-76223-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dcf/5652700/ad4b31375e8c/oncotarget-08-76223-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dcf/5652700/40d6bebb4c2d/oncotarget-08-76223-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dcf/5652700/0ff7d70d551d/oncotarget-08-76223-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dcf/5652700/7d162158bd88/oncotarget-08-76223-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dcf/5652700/ca9377be7e73/oncotarget-08-76223-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dcf/5652700/fb4390ac692a/oncotarget-08-76223-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dcf/5652700/ad4b31375e8c/oncotarget-08-76223-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dcf/5652700/40d6bebb4c2d/oncotarget-08-76223-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dcf/5652700/0ff7d70d551d/oncotarget-08-76223-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dcf/5652700/7d162158bd88/oncotarget-08-76223-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dcf/5652700/ca9377be7e73/oncotarget-08-76223-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dcf/5652700/fb4390ac692a/oncotarget-08-76223-g006.jpg

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Oncotarget. 2016 Jun 28;7(26):40377-40386. doi: 10.18632/oncotarget.9750.
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Pharmaceutics. 2022 Jun 29;14(7):1380. doi: 10.3390/pharmaceutics14071380.
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