Sox17 regulates proliferation and cell cycle during gastric cancer progression

Sox17, a transcription factor, was considered as an antagonist to inhibit canonical Wnt/β-catenin signaling in several malignant tumors. Extremely little is known about Sox17 in gastric cancer. Therefore, the aim of this study was to elucidate the vital role of Sox17 in the tumorigenesis and progression of gastric cancer. Real time PCR was used to detect the expression of Sox17 in gastric cancer tissue. Furthermore, a series of function assays, utilizing small interfering RNA (siRNA)-mediated knockdown of Sox17 expression in MKN45 gastric cancer cells, have been performed in this study, including proliferation assay, clonogenic assay, cell-cycle evaluation, apoptosis detection as well as western blot assay. Sox17 expression were low in gastric cancer tissues as compared to normal tissue (P = 0.013). Knockdown of Sox17 by Sox17-siRNA markedly enhanced the proliferation ability of MKN45 cells when compared with negative siRNA-infected cells and mock group (P < 0.05). Down-regulation of Sox17 contributed to increasing cloning efficiency and activating cell cycle of MKN45 cells (P < 0.05). However, there was no significantly statistical difference in terms of apoptosis rate between Sox17-siRNA group and Negative or mock group. Western blot assay revealed that the expression of CyclinD1 observably increased while p27Kip1 expression remarkably decreased in MKN45 cells with Sox17-siRNA transfection. Furthermore, apoptosis-related molecules, Caspase3 and Bcl-xl, have no dramatically discrepant expression when knockdown of Sox17 in MKN45 cells. Sox17 prominently contributes to gastric cancer progression through regulating proliferation and cell cycle, indicating a novel diagnosis and prognosis biomarker as well as a potential therapeutic target in gastric cancer.