PEKARČÍKOVÁ, Lucie, Lucia KNOPFOVÁ, Petr BENEŠ and Jan ŠMARDA. c-Myb regulates NOX1/p38 to control survival of colorectal carcinoma cells. Online. Cellular Signalling. New York, USA: Elsevier Science, 2016, vol. 28, No 8, p. 924-936. ISSN 0898-6568. Available from: https://dx.doi.org/10.1016/j.cellsig.2016.04.007. [citováno 2024-04-24]
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Basic information
Original name c-Myb regulates NOX1/p38 to control survival of colorectal carcinoma cells
Name in Czech c-Myb řídí přežívání buněk kolorektálního karcinomu prostřednictvím NOX1/p38
Authors PEKARČÍKOVÁ, Lucie (203 Czech Republic, belonging to the institution), Lucia KNOPFOVÁ (203 Czech Republic, belonging to the institution), Petr BENEŠ (203 Czech Republic, belonging to the institution) and Jan ŠMARDA (203 Czech Republic, guarantor, belonging to the institution)
Edition Cellular Signalling, New York, USA, Elsevier Science, 2016, 0898-6568.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 10601 Cell biology
Country of publisher United States of America
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 3.937
RIV identification code RIV/00216224:14310/16:00088855
Organization unit Faculty of Science
Doi http://dx.doi.org/10.1016/j.cellsig.2016.04.007
UT WoS 000378670900015
Keywords (in Czech) kolorektální karcinom; c-Myb; NADPH oxidáza; přežívání buněk; reaktivní kyslíkové radikály; signální dráha
Keywords in English Colorectal carcinoma; c-Myb; NADPH oxidase; Cell survival; Reactive oxygen species; Signaling pathway
Tags AKR
Tags International impact, Reviewed
Changed by Changed by: doc. Mgr. Petr Beneš, Ph.D., učo 2082. Changed: 19/2/2018 09:59.
Abstract
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.
Links
NT13441, research and development projectName: Exprese proteinů rodiny Myb v adenokarcinomech tlustého střeva a vztah k jejich metastatickému potenciálu
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