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.
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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 |
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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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