Premium
Attenuation of Smad2 activity shows resistance to TGF‐β signalling in mammary adenocarcinoma (MCF‐7) cells
Author(s) -
Sengupta Suman,
Kundu Subhadip,
Bhattacharyya Arindam
Publication year - 2013
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10061
Subject(s) - transforming growth factor , phosphorylation , cancer research , transforming growth factor beta , smad2 protein , context (archaeology) , downregulation and upregulation , mcf 7 , kinase , microbiology and biotechnology , chemistry , biology , cancer cell , cancer , biochemistry , gene , human breast , genetics , paleontology
Transforming growth factor‐β (TGF‐β) is a potent inhibitor of the growth of normal mammary epithelial cells, and has a pleiotropic, context‐dependent, concentration‐dependent action. We found attenuation of TGF‐β signalling in mammary adenoma carcinoma cells. Phosphorylation at the linker site of Smad2 occurred in a cooperative way during the attenuation of TGF‐β signalling, and was associated with upregulation of CDK2 and cyclin D1. CDK2 inhibitor restored the anti‐proliferative effect of TGF‐β by upregulating p21, with inhibition of linker phosphorylation of Smad2. CDK2‐mediated linker phosphorylation of Smad2 may be a plausible mechanism for the attenuation of TGF‐β signalling in breast cancer.