Estrogen-dependent activation of NCOA3 couples with p300 and NF-κB to mediate antiapoptotic genes in ER-positive breast cancer cells.

ABSTRACT: Circumvention of apoptosis by the elevation of antiapoptotic proteins is an important cause of carcinogenesis. The induction of antiapoptotic genes, including B-cell CLL/lymphoma 2 (BCL2), BCL2 related protein A1 (BCL2A1), BCL2 like 1 (BCL2L1), BCL2L2, and myeloid cell leukemia 1 (MCL1), has been observed in multiple cancers, including breast cancer. However, the underlying mechanisms of their overexpression are still being investigated. Here, we revealed that BCL2, BCL2A1, BCL2L2, and MCL1 but not BCL2L1 were overexpressed in estrogen receptor (ER)-positive breast cancer cells and clinical biopsies. Stimulation with estrogen in ER-positive cell lines resulted in a dose-dependent increase in BCL2, BCL2A1, BCL2L2, and MCL1 mRNA levels. Molecular investigation revealed that nuclear factor ka

SUBMITTER: Wang J 

PROVIDER: S-EPMC9975134 | biostudies-literature | 2023 Feb

REPOSITORIES: biostudies-literature