Oncotarget

Research Papers:

YY1 promotes HDAC1 expression and decreases sensitivity of hepatocellular carcinoma cells to HDAC inhibitor

Sheng Dong _, Xiang Ma, Zusen Wang, Bing Han, Hao Zou, Zehua Wu, Yunjin Zang and Likun Zhuang

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Oncotarget. 2017; 8:40583-40593. https://doi.org/10.18632/oncotarget.17196

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Abstract

Sheng Dong1, Xiang Ma1, Zusen Wang1, Bing Han1, Hao Zou1, Zehua Wu1, Yunjin Zang2 and Likun Zhuang2

1Department of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, Qingdao, 266003, China

2Institute of Transplantation Science, The Affiliated Hospital of Qingdao University, Qingdao, 266003, China

Correspondence to:

Likun Zhuang, email: zlk0823@163.com

Yunjin Zang, email: zangyunjin12@163.com

Keywords: YY1, HDAC1, HDAC inhibitor, HCC, drug sensitivity

Received: February 20, 2017     Accepted: April 05, 2017     Published: April 18, 2017

ABSTRACT

YY1 is a DNA-binding transcription factor and reported to be involved in cancer progression. Histone deacetylase inhibitor (HDACi) could inhibit proliferation and promote apoptosis of Hepatocellular carcinoma (HCC) cells. However, it is unclear about the roles of YY1 in the sensitivity of HCC cells to HDACi. In this study, firstly, we identified two drug-response profiles to HDACi in HCC cell lines, while our results showed that HDAC1 expression was positively correlated with YY1 in HCC cell lines and primary tumor tissues. Secondly, YY1 decreased the sensitivity of HCC cells to HDACi in vitro and in vivo. Furthermore, we found that YY1 promoted HDAC1 expression by binding to its promoter, while HDAC1 in turn up-regulated the expression of YY1. In conclusion, our results showed that YY1 could reduce the sensitivity of HCC cells to HDACi and might be a potential therapeutic target in HCC.


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PII: 17196