Mitochondrial estrogen receptor β inhibits non-small cell lung cancer cell apoptosis via interaction with Bad.
- Author:
Qiang XIE
1
;
Zuoping HUANG
;
Ying LIU
;
Xiao LIU
;
Lei HUANG
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; Carcinoma, Non-Small-Cell Lung; pathology; Cell Line, Tumor; Cisplatin; Estrogen Receptor beta; metabolism; Humans; Mitochondrial Proteins; metabolism; bcl-Associated Death Protein; metabolism
- From: Journal of Southern Medical University 2015;35(1):98-102
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the molecular mechanisms by which mitochondrial estrogen receptor β (ERβ) suppresses non-small cell lung cancer cell apoptosis induced by apoptotic stimulations.
METHODSThe mitochondrial localization of ERβ in non-small cell lung cancer cell lines A549 and 201T was determined using immunofluorescence and Western blotting. The changes of apoptosis of the cells with mitochondrial ERβ overexpression or knockdown in response to cisplatin and STS treatments were assessed, and mitochondrial ERβ interaction with the pro-apoptotic protein Bad was detected using co-immunoprecipitation and Western blotting.
RESULTSERβ was localized in the mitochondria in A549 and 201T cells. ERβ overexpression significantly reduced while ERβ knockdown increased Bax activation and cell apoptosis induced by cisplatin and STS. Mitochondrial ERβ interaction with pro-apoptotic protein Bad may suppress Bax activation and its translocation to the mitochondria.
CONCLUSIONMitochondrial ERβ can suppress apoptosis of non-small cell lung cancer cells induced by cisplatin or STS through interaction with Bad, suggesting the value of mitochondrial ERβ as a new therapeutic target for treatment of non-small cell lung cancer.