p53 inactivation decreases dependence on estrogen/ERK signalling for proliferation but promotes EMT and susceptility to 3-bromopyruvate in ERα+ breast cancer MCF-7 cells.

Conclusions.- a) ERα(+) breast cancer cells dysfunctional for TP53 which proliferate irrespective of low estrogen and chemical MEK inhibition are likely to increase metabolic consumption becoming increasingly susceptible to 3-BrPA; b) targeting the pyruvate pathway may improve response to endocrine therapy in ERα(+) breast cancer with p53 dysfunction. PMID: 24486524 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/24486524?dopt=Abstract

Source: Biochemical Pharmacology - January 28, 2014 Category: Drugs & Pharmacology Authors: Rieber M, Strasberg-Rieber M Tags: Biochem Pharmacol Source Type: research