Identification of molecules mediating c-myb-dependent chemoresistance of colorectal carcinoma cells

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Year of publication 2015
Type Conference abstract
MU Faculty or unit

Faculty of Science

Description Colorectal carcinoma (CRC) is the third most common cancer worldwide. High c-Myb expression is frequently associated with a variety of immature cell lineages, and it decreases as cells differentiate. Patients with colorectal carcinomas exhibiting upregulated c-Myb expression have poor prognosis. The aim of our study was to clarify the role of c-Myb in control of the cell death/survival of CRC cells treated with cytotoxic agents. We showed that c-Myb reduced sensitivity of CRC cells to the cytotoxic agents. We tested the levels of ROS and expression/activity of key components of several signalling pathways to identify downstream effectors mediating the effect of c-Myb on cell viability. We identified the enhanced levels of (a) ROS-generating NADPH oxidase (NOX), (b) the phosphorylated MAPKp38, and (c) JNK/c-Jun kinases upon c-Myb overexpression. In this work we documented for the first time that the prosurvival effect of c-Myb is associated with NOX1-dependent regulation of ROS and we discuss the role of c-Myb-ROS axis in activation of MAPKp38 and c-Jun kinases.
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