Kumari , R. and Chouhan , S. and Singh , S. and Chhipa , R.R and Ajay , A.K. and Bhat , M.K (2017) Constitutively activated ERK sensitizes cancer cells to doxorubicin: Involvement of p53-EGFR-ERK pathway. Journal of Bioscience, 42 (1). pp. 31-41. ISSN 42(1):31-41.

Text 48.Dr. Bhat M.K. (J. Bioscience) rest.pdf Restricted to Registered users only Download (820Kb) | Request a copy

Abstract

The tumour suppressor gene p53 is mutated in approximately 50% of the human cancers. p53 is involved in genotoxic stress-induced cellular responses. The role of EGFR and ERK in DNA-damage-induced apoptosis is well known. We investigated the involvement of activation of ERK signalling as a consequence of non-functional p53, in sensitivity of cells to doxorubicin. We performed cell survival assays in cancer cell lines with varying p53 status: MCF-7 (wild-type p53, WTp53), MDA MB-468 (mutant p53, MUTp53), H1299 (absence of p53, NULLp53) and an isogenic cell line MCF-7As (WTp53 abrogated). Our results indicate that enhanced chemosensitivity of cells lacking wild-type p53 function is because of elevated levels of EGFR which activates ERK. Additionally, we noted that independent of p53 status, pERK contributes to doxorubicin-induced cell death.

Item Type:	Article
Subjects:	Insect Molecular Biology
Depositing User:	Mr. Rameshwar Nema
Date Deposited:	24 Apr 2017 09:48
Last Modified:	02 Mar 2021 12:08
URI:	http://nccs.sciencecentral.in/id/eprint/414

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