Hepatic SIRT6 deficit promotes liver tumorigenesis in the mice models

Mei Wang; Linhua Lan; Fan Yang; Shan Jiang; Haojun Xu; Chengfei Zhang; Guoren Zhou; Hongping Xia; Jinglin Xia

doi:10.1016/j.gendis.2020.08.007

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Hepatic SIRT6 deficit promotes liver tumorigenesis in the mice models

更新时间：2022-06-24

- Hepatic SIRT6 deficit promotes liver tumorigenesis in the mice models
- Genes & Diseases Vol. 9, Issue 3, (2022)
- 作者机构：
  
  1. Department of Pathology in the School of Basic Medical Sciences & Sir Run Run Hospital & State Key Laboratory of Reproductive Medicine & Key Laboratory of Antibody Technique of National Health Commission, Nanjing Medical University,Jiangsu,Nanjing,PR China,211166
  2. Department of Immunology, Medical School of Southeast University,Jiangsu,Nanjing,PR China,210009
  3. The First Affiliated Hospital of Wenzhou Medical University,Zhejiang,Wenzhou,PR China,325000
  4. The First Affiliated Hospital of Chongqing Medical University,Chongqing,PR China,400016
  5. Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University,Jiangsu,Nanjing,PR China,210009
- 作者简介：
- 基金信息：
- DOI：10.1016/j.gendis.2020.08.007
  CLC：
- Published：2022，
  
  Published Online：1 May 2022，
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Mei Wang, Linhua Lan, Fan Yang, et al. Hepatic SIRT6 deficit promotes liver tumorigenesis in the mice models. [J]. Genes & Diseases 9(3).(2022)
DOI：

Mei Wang, Linhua Lan, Fan Yang, et al. Hepatic SIRT6 deficit promotes liver tumorigenesis in the mice models. [J]. Genes & Diseases 9(3).(2022) DOI： 10.1016/j.gendis.2020.08.007.

摘要

Abstract

SIRT6 belongs to class III sirtuin family with NAD+-dependent histone deacetylase activities and controls multiple processes including aging

metabolism and inflammation. In recent years

increasing studies showed tumor suppressor role of SIRT6 in HCC development. We established a two-stage DEN followed CCl4 induced liver carcinogenesis in the hepatic-specific SIRT6 HKO mice models and found that hepatic SIRT6 deficit significantly promotes liver injury and liver cancer through inhibition of the ERK1/2 pathway. SIRT6 was compensatory upregulated in mice tumor tissues and human HCC cells and overexpressed SIRT6 inhibits tumor growth both

in vitro

and

in vivo

. Taken together

we provide a useful mouse model for delineating the molecular pathways involved in chronic liver diseases and primary liver cancer and suggest that SIRT6 can be a promising target for HCC therapies.

关键词

Keywords

ERK1/2 pathwayHCCLiver carcinogenesisMouse modelSIRT6

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