Inhibition of survivin enhances radiosensitivity of esophageal cancer cells by switching radiation-induced senescence to apoptosis

• DOI: 10.2147/ott.s166798
• Publication Date: 2018-05-23T23:55:31Z
• Authors: Xianghe Liu; Yahui Zhao; Weina Zhang; Yang Gao; Miaomiao Huo; Mei Liu; Zefen Xiao; Shufang Liang; Ningzhi Xu; Hongxia Zhu
• Keywords: Radiosensitivity; Survivin; Propidium iodide; Senescence; Clonogenic assay

Strategies to increase radiosensitivity are urgently needed. Combining radiosensitizing reagents with radiotherapy could improve the outcome of cancer treatment. Some preclinical studies showed that sepantronium bromide (YM155) sensitize cells radiation by inhibiting survivin protein. In this study, we try investigate function YM155 on esophageal squamous cell carcinoma (ESCC) cells.ESCC lines were treated and YM155, efficacy was evaluated counting kit-8 assay clonogenic survival assay. Cell senescence measured senescence-associated β-galactosidase staining. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay, fluorescein isothiocyanate-labeled Annexin V/propidium iodide poly ADP-ribose polymerase cleavage used detect apoptosis. KYSE150 xenografts model test combined YM155.YM155 inhibit upregulation induced in all ESCC lines, but radiosensitization varied different lines. Radiation-induced KYSE410 cells, combination inhibited promoted apoptosis thereby enhancing radiosensitivity. Combination delayed growth nude mice switching radiation-induced When p21 did not induce senescence, also attenuated. KYSE510 KYSE180 enhance radiosensitivity.Our results suggest a new mechanism might The major determinant be induction radiation.