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Myc stabilization in response to estrogen and phospholipase D in MCF‐7 breast cancer cells
Author(s) -
Rodrik Vanessa,
Gomes Evan,
Hui Li,
Rockwell Patricia,
Foster David A.
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.09.013
Subject(s) - mcf 7 , estrogen , breast cancer , cancer research , estrogen receptor , estrogen receptor beta , apoptosis , medicine , estrogen receptor alpha , endocrinology , cancer , phospholipase d , phosphorylation , cancer cell , chemistry , biology , signal transduction , microbiology and biotechnology , biochemistry , human breast
Estrogen, which has been strongly implicated in breast cancer, suppresses apoptosis in estrogen receptor (ER) positive MCF‐7 breast cancer cells. Phospholipase D (PLD), which is commonly elevated in ER negative breast cancer cells, also suppresses apoptosis. Survival signals generated by both estrogen and PLD are dependent upon elevated Myc expression. We report here that estrogen‐ and PLD‐induced increases in Myc expression are due to reduced turnover of Myc protein. Estrogen and PLD suppressed phosphorylation of Myc at Thr58 – a site that targets Myc for degradation by the proteasome. The data provide a mechanism for elevated Myc expression in hormone‐dependent and hormone‐independent breast cancer.