Attenuation of Smad2 activity shows resistance to TGF‐β signalling in mammary adenocarcinoma (MCF‐7) cells. (13th March 2013)

• Record Type: Journal Article
• Authors: Sengupta, Suman; Kundu, Subhadip; Bhattacharyya, Arindam
• Is Part Of: Cell biology international. Volume 37:Number 5(2013)
• Page Start: 449
• Page End: 457
• Publication Date: 2013-03-13
• Subjects: Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.10061
• Languages: English
• ISSNs: 1065-6995

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <sec id="cbin10061-sec-0001" sec-type="section"> <p>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.</p> </sec> </abstract>