c-Myb regulates NOX1/p38 to control survival of colorectal carcinoma cells
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
27107996
DOI
10.1016/j.cellsig.2016.04.007
PII: S0898-6568(16)30092-4
Knihovny.cz E-zdroje
- Klíčová slova
- Cell survival, Colorectal carcinoma, NADPH oxidase, Reactive oxygen species, Signaling pathway, c-Myb,
- MeSH
- aktivace enzymů účinky léků MeSH
- apoptóza účinky léků MeSH
- cisplatina farmakologie MeSH
- doxorubicin farmakologie MeSH
- kolorektální nádory genetika patologie MeSH
- lidé MeSH
- messenger RNA genetika metabolismus MeSH
- mitogenem aktivované proteinkinasy p38 genetika metabolismus MeSH
- myši MeSH
- NADH, NADPH oxidoreduktasy genetika metabolismus MeSH
- nádorové buněčné linie MeSH
- NADPH-oxidasa 1 MeSH
- NADPH-oxidasy genetika metabolismus MeSH
- organoplatinové sloučeniny farmakologie MeSH
- oxaliplatin MeSH
- oxidační stres účinky léků MeSH
- promotorové oblasti (genetika) genetika MeSH
- protoonkogenní proteiny c-myb metabolismus MeSH
- reaktivní formy kyslíku metabolismus MeSH
- regulace genové exprese u nádorů * účinky léků MeSH
- sekvence nukleotidů MeSH
- upregulace účinky léků MeSH
- vazebná místa MeSH
- viabilita buněk MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- cisplatina MeSH
- doxorubicin MeSH
- messenger RNA MeSH
- mitogenem aktivované proteinkinasy p38 MeSH
- NADH, NADPH oxidoreduktasy MeSH
- NADPH-oxidasa 1 MeSH
- NADPH-oxidasy MeSH
- NOX1 protein, human MeSH Prohlížeč
- NOX1 protein, mouse MeSH Prohlížeč
- organoplatinové sloučeniny MeSH
- oxaliplatin MeSH
- protoonkogenní proteiny c-myb MeSH
- reaktivní formy kyslíku MeSH
The c-Myb transcription factor is important for maintenance of immature cells of many tissues including colon epithelium. Overexpression of c-Myb occurring in colorectal carcinomas (CRC) as well as in other cancers often marks poor prognosis. However, the molecular mechanism explaining how c-Myb contributes to progression of CRC has not been fully elucidated. To address this point, we investigated the way how c-Myb affects sensitivity of CRC cells to anticancer drugs. Using CRC cell lines expressing exogenous c-myb we show that c-Myb protects CRC cells from the cisplatin-, oxaliplatin-, and doxorubicin-induced apoptosis, elevates reactive oxygen species via up-regulation of NOX1, and sustains the pro-survival p38 MAPK pathway. Using pharmacological inhibitors and gene silencing of p38 and NOX1 we found that these proteins are essential for the protective effect of c-Myb and that NOX1 acts upstream of p38 activation. In addition, our result suggests that transcription of NOX1 is directly controlled by c-Myb and these genes are strongly co-expressed in human tumor tissue of CRC patients. The novel c-Myb/NOX1/p38 signaling axis that protects CRC cells from chemotherapy described in this study could provide a new base for design of future therapies of CRC.
Citace poskytuje Crossref.org
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