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      https://www.ias.ac.in/article/fulltext/jbsc/042/01/0031-0041

    • Keywords

       

      Doxorubicin; EGFR; ERK; p53

    • Abstract

       

      The tumour suppressor gene p53 is mutated in approximately 50% of the human cancers. p53 is involved in genotoxicstress-induced cellular responses. The role of EGFR and ERK in DNA-damage-induced apoptosis is well known. Weinvestigated the involvement of activation of ERK signalling as a consequence of non-functional p53, in sensitivity ofcells to doxorubicin. We performed cell survival assays in cancer cell lines with varying p53 status: MCF-7 (wild-typep53, WTp53), MDA MB-468 (mutant p53, MUTp53), H1299 (absence of p53, NULLp53) and an isogenic cell lineMCF-7As (WTp53 abrogated). Our results indicate that enhanced chemosensitivity of cells lacking wild-type p53function is because of elevated levels of EGFR which activates ERK. Additionally, we noted that independent of p53status, pERK contributes to doxorubicin-induced cell death.

    • Author Affiliations

       

      RATNA KUMARI1 SURBHI CHOUHAN1 SNAHLATA SINGH1 RISHI RAJ CHHIPA1 AMRENDRA KUMAR AJAY1 MANOJ KUMAR BHAT1

      1. National Centre for Cell Science, Savitribai Phule Pune University Campus, Ganeshkhind, Pune 411 007, India
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  • Journal of Biosciences | News

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