Suppression of estrogen receptor-beta promotes gastric cancer cell apoptosis with induction of autophagy.

ABSTRACT: Estrogen Receptor 2 (ESR2) is the protein-coding gene of estrogen receptor β (ERβ) and has been shown to be abundantly expressed in gastric carcinoma (GC), suggesting that it plays a role in GC pathogenesis. However, the underlying molecular mechanism remains elusive. In the present in vitro study, GC cell growth was found to be estrogen-dependent, and the expression level of ERβ was higher than that of ERα. Knocking down the endogenous expression of ESR2 in GC cells increased the apoptosis rate and the level of cleaved caspase-3, caspase-7 and poly ADP-ribose polymerase. The induced apoptosis was primarily related to GC cell growth arrest, accompanied with activation of DNA damage-inducible protein 45 alpha (GADD45α) in a p53-independent manner. Importantly, down-regulation of ESR2

SUBMITTER: Zhou F 

PROVIDER: S-EPMC7476128 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature