Inhibition of redox/Fyn/c-Cbl pathway function by Cdc42 controls tumour initiation capacity and tamoxifen sensitivity in basal-like breast cancer cells.
Ontology highlight
ABSTRACT:
SUBMITTER: Chen HY
PROVIDER: S-EPMC3662315 | biostudies-other | 2013 May
REPOSITORIES: biostudies-other
Publications
Inhibition of redox/Fyn/c-Cbl pathway function by Cdc42 controls tumour initiation capacity and tamoxifen sensitivity in basal-like breast cancer cells.
Chen Hsing-Yu HY Yang Yin M YM Stevens Brett M BM Noble Mark M
EMBO molecular medicine 20130422 5
We found that basal-like breast cancer (BLBC) cells use Cdc42 to inhibit function of the redox/Fyn/c-Cbl (RFC) pathway, which normally functions to convert small increases in oxidative status into enhanced degradation of c-Cbl target proteins. Restoration of RFC pathway function by genetic or pharmacological Cdc42 inhibition enabled harnessing of pro-oxidant effects of low µM tamoxifen (TMX) concentrations - concentrations utilized in trials on multiple tumour types - to suppress division and in ...[more]
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