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Attenuation of Smad2 activity shows resistance to TGF-β signalling in mammary adenocarcinoma (MCF-7) cells

Authors

  • Suman Sengupta,

    1. Immunology Lab, Department of Zoology, University of Calcutta, Kolkata, West Bengal, India
    2. Department of Environmental Science, University of Kalyani, West Bengal, India
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  • Subhadip Kundu,

    1. Immunology Lab, Department of Zoology, University of Calcutta, Kolkata, West Bengal, India
    2. Department of Environmental Science, University of Kalyani, West Bengal, India
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  • Arindam Bhattacharyya

    Corresponding author
    • Immunology Lab, Department of Zoology, University of Calcutta, Kolkata, West Bengal, India
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Corresponding author: e-mail: arindam19@yahoo.com

Abstract

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.

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