Promoter methylation and H3K27 deacetylation regulate the transcription of VIPR1 in hepatocellular carcinoma

被引：14
|
作者：
Lu, Sicong [2 ]
Lu, Haiming [2 ]
Jin, Rongzhong [1 ]
Mo, Zhijing [1 ]
机构：
[1] Guilin Med Univ, Coll Biotechnol, Guilin 541100, Guangxi Zhuang, Peoples R China
[2] Liu Zhou Workers Hosp, Dept Hepatobiliaty, Surg Dept, Liuzhou 545005, Guangxi Zhuang, Peoples R China
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2019年 / 509卷 / 01期
基金：
中国国家自然科学基金;
关键词：
VIPR1; Methylation; Deacetylation; HCC; Prognosis; EXPRESSION; DATABASE; CELLS;
D O I：
10.1016/j.bbrc.2018.12.129
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Vasoactive intestinal peptide receptor 1 (VIPR1) is observed to express differently in human malignancies. Here, we aim to reveal clinical significance and transcriptional regulation mechanism of VIPR1 in hepatocellular carcinoma (HCC). Using immunohistochemistry, pyrosequencing, quantitative real-time PCR (qPCR), decitabine (DAC)/4-phenylbutyricacid (PBA) treatment and chromatin immunoprecipitation (ChIP), we found the low expression of VIPR1 was correlated with poor histological differentiation and poor survival. The promoter region of VIPR1 was methylated and DNA methylation inhibited VIPR1 gene transcription. Deacetylation of H3K27 in the promoter of VIPR1 inhibited the transcription of VIPR1 in HCC. In conclusion, low expression of VIPR1 had an adverse prognostic impact on HCC, and such expression is at least partially mediated by epigenetic modification. (C) 2018 Elsevier Inc. All rights reserved.
引用
收藏
页码：301 / 305
页数：5
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