PEKARČÍKOVÁ, Lucie, Lucia KNOPFOVÁ, Petr BENEŠ, Markéta HERMANOVÁ, Michal TICHÝ and Jan ŠMARDA. The c-Myb-induced resistance of colon cancer cells to cisplatin is mediated by the p38 MAP kinase. In Korean Journal of Pathology. 2013. ISSN 1738-1843.
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Basic information
Original name The c-Myb-induced resistance of colon cancer cells to cisplatin is mediated by the p38 MAP kinase
Name in Czech Rezistence buněk střevního karcinomu k cisplatině indukovaná proteinem c-Myb je zprostředkovaná MAP kinázou p38
Name (in English) The c-Myb-induced resistance of colon cancer cells to cisplatin is mediated by the p38 MAP kinase
Authors PEKARČÍKOVÁ, Lucie, Lucia KNOPFOVÁ, Petr BENEŠ, Markéta HERMANOVÁ, Michal TICHÝ and Jan ŠMARDA.
Edition Korean Journal of Pathology, 2013.
Other information
Type of outcome Conference abstract
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 0.174 in 2012
ISSN 1738-1843
Changed by Changed by: Ing. Mgr. Věra Pospíšilíková, učo 9005. Changed: 20/4/2015 10:49.
Abstract
Background: The c-Myb transcription factor is essential for maintenance of stem-progenitor cells in colon epithelia and its expression is deregulated in premalignant adenomatous polyps and colorectal carcinomas. Patients with colorectal carcinoma exhibiting upregulated c- Myb expression have poor prognosis. This can result from low sensitivity of cancer cells to cytotoxic agents. Methods: In our study, increased resistance of colon carcinoma CT26 and HCT116 cells overproducing exogenous c-Myb to cytotoxic agents was observed. These cells lost sensitivity to cisplatin and doxorubicin upon upregulation of c-Myb. The effect of c-Myb can be mediated by the mitogen-activated protein kinase (MAPK) signaling since phosphorylation of the MAPKs p38 and JNK was enhanced in cells exhibiting high expression of exogenous c-Myb. Results: To determine functional contribution of these kinases to resistance of the c-Myb-overexpressing cells to cisplatin, we used BIRB796 to inhibit activity of p38 and SP600125 to inhibit JNK. We found that the c-Myb-induced resistance of CT26 cells to cisplatin can be reversed by BIRB796. Conclusions: This result documents that it is the p38 kinase that mediates the effects of c-Myb on sensitivity of colon cancer CT26 cells to cisplatin (This study was supported by grant NT13441/2012 of the Internal Grant Agency of the Ministry of Health, Czech Republic).
Abstract (in English)
Background: The c-Myb transcription factor is essential for maintenance of stem-progenitor cells in colon epithelia and its expression is deregulated in premalignant adenomatous polyps and colorectal carcinomas. Patients with colorectal carcinoma exhibiting upregulated c- Myb expression have poor prognosis. This can result from low sensitivity of cancer cells to cytotoxic agents. Methods: In our study, increased resistance of colon carcinoma CT26 and HCT116 cells overproducing exogenous c-Myb to cytotoxic agents was observed. These cells lost sensitivity to cisplatin and doxorubicin upon upregulation of c-Myb. The effect of c-Myb can be mediated by the mitogen-activated protein kinase (MAPK) signaling since phosphorylation of the MAPKs p38 and JNK was enhanced in cells exhibiting high expression of exogenous c-Myb. Results: To determine functional contribution of these kinases to resistance of the c-Myb-overexpressing cells to cisplatin, we used BIRB796 to inhibit activity of p38 and SP600125 to inhibit JNK. We found that the c-Myb-induced resistance of CT26 cells to cisplatin can be reversed by BIRB796. Conclusions: This result documents that it is the p38 kinase that mediates the effects of c-Myb on sensitivity of colon cancer CT26 cells to cisplatin (This study was supported by grant NT13441/2012 of the Internal Grant Agency of the Ministry of Health, Czech Republic).
Links
NT13441, research and development projectName: Exprese proteinů rodiny Myb v adenokarcinomech tlustého střeva a vztah k jejich metastatickému potenciálu
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