RESUMO
Survivin and transcription factor p65 (NFκB p65) participate in the progression of esophageal squamous cell carcinoma (ESCC). However, the mechanism of NFκB p65 activation in ESCC remains to be elucidated. The aim of the present study was to investigate the role of survivin in the activation of NFκB p65 in ESCC. The expression levels of survivin, NFκB p65, inhibitor of nuclear factor κB kinase subunit α (IKKα) and inhibitor of nuclear factor κB kinase subunit ß (IKKß) were detected in ESCC tissue samples. Eca109 and KYSE150 cells were cultured and survivin activity was modulated via transfection with an overexpression plasmid, a small hairpin RNA plasmid and a specific inhibitor. Quantitative reverse transcription-polymerase chain reaction and western blotting assays were conducted to assess the effects of survivin on the expression levels of IKKα, IKKß and NFκB p65. Cell cycle and apoptosis assays were conducted to detect surviving-dependent cellular behavior changes. In addition, the luciferase reporter gene assay and chromatin immunoprecipitation assay were conducted to determine the genomic sites responsible for surviving-induced activation of NFκB p65. The present study demonstrated that the expression of survivin is positively correlated with IKKα and IKKß in ESCC tissues. Survivin affected the mRNA and protein expression levels of IKKα, IKKß, and NFκB p65 in Eca109 and KYSE150 cells. Furthermore, survivin increased the transcriptional activity of the IKKß promoter and bound to the IKKß promoter region in the Eca109 cells. Downregulation of survivin arrested the cell cycle at the G2/M phase and induced apoptosis. Results of the present study suggest that survivin activates NFκB p65 in Eca109 cells via binding to the IKKß promoter region and upregulating IKKß promoter transcriptional activity. Survivin overexpression activates NFκB p65, which is important in the acquisition and maintenance of the oncogenic characteristics of ESCC.