Expression profile of in gastric cells treated with bile acids. Homo sapiens

Bile reflux is one of the main causes of gastric intestinal metaplasia (IM) which is an important precancerous lesion. Our previous study has shown that ectopic expression of Histone deacetylase 6 (HDAC6) promotes the activation of intestinal markers in bile acids (BA) induced gastric IM cells; however, the mechanism underlying how HDAC6-mediated epigenetic modifications regulate intestinal markers is not clear. In this study, we aimed to investigate the downstream targets of HDAC6 and the underlying mechanism in the process of BA induced gastric IM. After HDAC6 overexpression or control treatment, GES-1 cells were detected by RNA-seq.

胆汁反流是胃肠上皮化生（gastric intestinal metaplasia, IM）的主要诱因之一，而胃肠上皮化生是一类重要的癌前病变。我们既往的研究显示，组蛋白去乙酰化酶6（HDAC6）的异位表达可促进胆汁酸（BA）诱导的胃IM细胞中肠标志物的激活；但HDAC6介导的表观遗传修饰调控肠标志物的具体分子机制尚未明确。本研究旨在探究胆汁酸诱导胃IM过程中HDAC6的下游靶点及其潜在调控机制。我们对HDAC6过表达处理及对照处理后的GES-1细胞进行了RNA测序（RNA-seq）检测。