Cisplatin is a common used chemotherapeutic
drug for the treatment of
laryngeal cancer. However, drug-resistance is a major obstacle in
platinum-based
chemotherapy for
laryngeal cancer. Recent studies have demonstrated that dysregulation of
microRNAs (
miRNAs) is responsible for chemoresistance in multiple
cancers including
laryngeal cancer, but the potential mechanisms are required to be explored. In the present study, we constantly exposed the
laryngeal cancer cell line Hep-2 with
cisplatin to establish a
cisplatin-resistant
laryngeal cancer cell model (Hep-2/R). We found that Hep-2/R cells exhibited obvious resistance to
cisplatin compared to the Hep-2 cells. However, overexpression of miR-26b significantly decreased the half maximal inhibitory concentration (IC50) of
cisplatin to Hep-2/R. Mechanically, miR-26b in Hep-2/R decreased the expression of ATF2, and thus inhibiting the phosphorylation of ATF2 and formation of cellular ATF2-c-Jun complex induced by
cisplatin. As the results, Hep-2/R cells failed to overexpress the Bcl-xl which is a key
anti-apoptotic protein under the
cisplatin treatment. Therefore, overexpression of miR-26b was found to be able to promote mitochondrial apoptosis induced by
cisplatin.