KRT17 Facilitates Proliferation, Migration and Invasion in Esophageal Squamous Cell Carcinoma by Regulating mTOR/S6K1 pathway

Abstract

BackgroundEsophageal squamous cell carcinoma (ESCC) is one of the most aggressive malignancies worldwide which originates from the malignant transformation of esophageal epithelial cells. Dysregulated expression of Keratin17 (KRT17) has been claimed in a variety of malignancies, while its role in ESCC remains unclear. Therefore, our study aimed to explore the potential function and underlying molecular mechanism of KRT17 in ESCC.MethodsData-independent acquisition-mass spectrometry (DIA-MS) workflow was used to analysis KRT17 expression between ESCC and adjacent non-cancerous esophageal tissues. The online database gene expression profiling interactive analysis (GEPIA) was used to further determine the differential expression of KRT17 in tissues. The function of KRT17 in ESCC was tested on two human esophageal cancer cell lines (EC9706 and ECA109). Small interfering RNA (siRNA) was used to inhibit KRT17 expression. Cell proliferation was examined by cell counting kit 8 (CCK8) reagent, colony formation assay, cell cycle distribution analysis and apoptosis. Cell migration was examined by transwell and wound healing assay. Cell invasion was also examined by transwell assay. Western blot and quantitative real-time PCR (qRT-PCR) was used to evaluate protein and mRNA levels, respectively.ResultsKRT17 expression was higher in cancer tissues compared with normal tissues. Transfected with siKRT17 attenuated protein and mRNA levels of KRT17, inhibited proliferation, migration and invasion, and decreased mTOR/S6K1 phosphorylation levels in EC9706 and ECA109.ConclusionKRT17 facilitates proliferation, migration and invasion in ESCC cells, and these cell viability functions were mediated by mTOR/S6K1 pathway.