Knockdown of LINC00857 Inhibits Cell Invasion and Migration and Induces Cell Apoptosis in Gastric Cancer via Wnt/beta-Catenin Signaling Pathway

摘要

Gastric cancer is the second major reason of cancer-associated mortalities, accompanied with a high rate of death worldwide every year. LncRNAs have been reported to be closely involved in the incidence and development of gastric cancer. Reports have shown an aberrant expression of LncRNA LINC00857 in various cancers, which is closely associated with the progression of cancers. The aim of our study is to further explore the role of LINC00857 and its potential mechanism of action in gastric cancer. The expression of LINC00857 in the normal gastric epithelial cell and four gastric cancer lines was detected by quantitative RT-PCR. After transfection with siRNA, cell proliferation ability was analyzed using colony formation assay and CCK-8 assay. The expressions of c-myc, bcl-2 and beta-catenin were determined by western blot and quantitative RT-PCR. Cell apoptosis was analyzed by flow cytometry. Besides, cell migration ability and invasive ability were determined by wounding-heal assay and Transwell assay, respectively. In this study, LINC00857 was upregulated in gastric cancer cells. Knockdown of LINC00857 obviously suppressed cell proliferation. The expressions of bcl-2, c-myc and beta-catenin were decreased when LINC00857 was downregulated. Additionally, knockdown of LINC00857 inhibited cell growth, migration and invasion, and promoting cell apoptosis, while Wnt/beta-catenin activator (SKL2001) could contrarily promote cell growth, migration and invasion, and inhibited cell apoptosis. Collectively, knockdown of LINC00857 could suppress cell growth, migration and invasion, and induce cell apoptosis by downregulating Wnt/beta-catenin signaling pathway in gastric cancer, providing novel insight for the therapy of gastric cancer.