HDAC is indispensable for IFN-γ-induced B7-H1 expression in gastric cancer
HDAC is indispensable for IFN-γ-induced B7-H1 expression in gastric cancer
复制标题
HDAC 对于 IFN-γ 诱导的胃癌中 B7-H1 表达是不可或缺的
DOI:
10.1186/s13148-018-0589-6
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发表时间:
2018-12-11
影响因子:
5.7
通讯作者:
Tao, Kaixiong
中科院分区:
文献类型:
--
作者:
Deng, Rui;Zhang, Peng;Tao, Kaixiong
BackgroundB7 homolog 1 (B7-H1) overexpression on tumor cells is an important mechanism of immune evasion in gastric cancer (GC). Elucidation of the regulation of B7-H1 expression is urgently required to guide B7-H1-targeted cancer therapy. Interferon gamma (IFN-) is thought to be the main driving force behind B7-H1 expression, and epigenetic factors including histone acetylation are recently linked to the process. Here, we investigated the potential role of histone deacetylase (HDAC) in IFN--induced B7-H1 expression in GC. The effect of Vorinostat (SAHA), a small molecular inhibitor of HDAC, on tumor growth and B7-H1 expression in a mouse GC model was also evaluated.ResultsRNA-seq data from The Cancer Genome Atlas revealed that expression of B7-H1, HDAC1-3, 6-8, and 10 and SIRT1, 3, 5, and 6 was higher, and expression of HDAC5 and SIRT4 was lower in GC compared to that in normal gastric tissues; that HDAC3 and HDAC1 expression level significantly correlated with B7-H1 in GC with a respective r value of 0.42 (p