Open AccessExpression of ERK1 and ERK2 in prostate cancer
Author(s) -
Norelia Torrealba,
Benito Fraile,
Gabriel Olmedilla,
Pilar Martínez-Onsurbe,
Manuel Guil-Cid,
Ricardo Paniagua,
Mar Royuela
Publication year - 2015
Publication title -
map kinase
Language(s) - English
Resource type - Journals
ISSN - 2235-4956
DOI - 10.4081/mk.2015.5265
Subject(s) - mapk/erk pathway , kinase , phosphorylation , prostate cancer , cancer research , mitogen activated protein kinase , signal transduction , receptor tyrosine kinase , tyrosine kinase , p38 mitogen activated protein kinases , biology , tyrosine phosphorylation , cancer , microbiology and biotechnology , medicine
Prostate cancer may emerge as result of dysregulated balance between cell proliferation and death rates, increased angiogenesis and chronic. These processes are regulated by numerous signaling proteins, including the mitogen-activated protein kinases (MAPKs). JNK, p38 and extracellular signal-regulated kinase (ERK) are the three major sub-families of MAPKs. The pro-oncogenic effects of ERK isoforms (ERK1 and ERK2) lie in their aberrant activation through phosphorylation by any mutation along the pathway of receptor tyrosine kinase (RTK)-Ras-Raf-MEK-ERK1/2. Once activated, ERKs phosphorylate cytoskeletal proteins, kinases, and transcription factors. Active ERK proteins induce strong proliferative and anti-apoptotic effects. Our group has tested variations in expression, activation and localization of ERKs in human prostate. Differential ERK1/2 expression and phosphorylation status may be linked to the progression of prostate cancer. The major striking observation is that ERKs are expressed in tumors with higher proportion than normal prostate. We believe that this is an important notion because the status (expression, localization, phosphorylation and the ERK1/ERK2 ratio) of ERK in the prostate may be developed into an important prognostic marker that predicts patient responce to the anti-cancer treatment