@article{Wang2022, 
author = {Mei Wang and Linhua Lan and Fan Yang and Shan Jiang and Haojun Xu and Chengfei Zhang and Guoren Zhou and Hongping Xia and Jinglin Xia},
title = {Hepatic SIRT6 deficit promotes liver tumorigenesis in the mice models},
year = {2022},
journal = {Genes & Diseases},
volume = {9},
number = {3},
pages = {789-796},
keywords = {ERK1/2 pathway, HCC, Liver carcinogenesis, Mouse model, SIRT6},
url = {https://www.sciopen.com/article/10.1016/j.gendis.2020.08.007},
doi = {10.1016/j.gendis.2020.08.007},
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.}
}