Targeting survivin with the small molecule sepantronium bromide (YM-155) in esophageal cancer

Background: Survivin is a member of the Inhibitor Apoptosis (IAP) protein family, and involved in regulation cell division inhibition apoptosis. Although survivin not expressed most normal human tissues, it has shown to be upregulated many cancers, including esophageal cancer. Based on its differential expression malignant tissues critical role regulating survival, an attractive candidate for targeted therapy. One promising therapeutic approaches targeting suppression transcription by small molecule inhibitor sepantronium bromide (YM-155). This agent demonstrated anti-tumor efficacy multiple malignancies, but cancer been evaluated. The goal this study determine YM-155 against broad panel lines. Material methods: Studies were performed lines TE7, TE10, OE21, SK-GT-4 epithelial line hESO. mRNA levels both XIAP, another IAP family member, measured real-time PCR. Protein was examined Western blot. Cellular viability following exposure assessed MTT assay. promoter activity luciferase reporter Results: Endogenous are markedly increased compared hESO cells. treatment effectively reduces all four with minimal effect XIAP expression. All exquisitely sensitive YM-155, ranges IC50 IC90 concentrations found lower than those reported other Exposure cells either or concentration results significant decrease activity. Conclusions: overexpressed decreased these YM-155. In addition, exposure, which suvivin dose-dependent manner. Our result suggest that interesting target treatment. No conflict interest.