Abstract:
:The MET receptor tyrosine kinase is deregulated primarily via overexpression or point mutations in various human cancers and different strategies for MET inhibition are currently evaluated in clinical trials. We observed by Western blot analysis and by Flow cytometry that MET inhibition by different MET small molecule inhibitors surprisingly increases in a dose-dependent manner total MET levels in treated cells. Mechanistically, this inhibition-related MET accumulation was associated with reduced Tyr1003 phosphorylation and MET physical association with the CBL ubiquitin ligase with concomitant decrease in MET ubiquitination. These data may suggest careful consideration for design of anti-MET clinical protocols.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Leiser D,Pochon B,Blank-Liss W,Francica P,Glück AA,Aebersold DM,Zimmer Y,Medová Mdoi
10.1016/j.febslet.2013.12.025subject
Has Abstractpub_date
2014-03-03 00:00:00pages
653-8issue
5eissn
0014-5793issn
1873-3468pii
S0014-5793(14)00019-2journal_volume
588pub_type
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