Open AccessCCN6: a novel method of aTAKing cancer
Author(s) -
Leask Andrew
Publication year - 2013
Publication title -
journal of cell communication and signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 44
eISSN - 1873-961X
pISSN - 1873-9601
DOI - 10.1007/s12079-012-0189-8
Subject(s) - medicine , matricellular protein , cancer research , ctgf , cancer , breast cancer , smad , protein kinase b , signal transduction , transforming growth factor , biology , extracellular matrix , receptor , growth factor , biochemistry , microbiology and biotechnology
It is well‐established that the expression of CCN family of matricellular proteins is altered in essentially all cancers and, hence, targeting these proteins may be a novel therapeutic approach to treating these diseases. For example, CCN6 (WISP3) is downregulated in aggressive breast cancers, and this phenomenon appears to result in the tumor survival by promoting Akt phosphorylation. In a recent report by Pal et al. (Cancer Res 72(18):4818‐4828, 2012), CCN6 knockdown was shown to promote BMP4‐mediated activation of the Smad‐independent TAK1 and p38 kinases. CCN6 expression was inversely associated with BMP4 and phospho‐p38 levels in 69 % of invasive breast carcinomas. TAK1 inhibition has been previously shown to decrease tumor progression in preclinical models of TAK1‐dependent cancers. These data are consistent with the idea that CCN6 may represent a novel therapeutic approach, as compared to attacking TAK1 directly, to selectively target breast cancers.