LINC01857 promotes the development of gastric cancer by regulating microRNA-200b.

Abstract

The aim of this study was to investigate the expression characteristics of LINC01857 in gastric cancer (GCa), and to further study whether it could promote GCa development by modulating microRNA-200b. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to examine LINC01857 expression in 60 pairs of GCa tissues and adjacent tissues. The interplay between LINC01857 level and clinical indexes and the prognosis of GCa patients was analyzed. Meanwhile, qRT-PCR was used to verify the expression level of LINC01857 in GCa cell lines. LINC01857 knockdown model was constructed by lentivirus transfection in GCa cell lines. Subsequently, the effect of LINC01857 on the biological function of GCa cells was analyzed by Cell Counting Kit 8 (CCK8), wound healing, and transwell assays. Furthermore, the in-depth relationship between LINC01857 and microRNA-200b was explored. QRT-PCR results showed that LINC01857 level in GCa tissues was remarkably higher than that of adjacent tissues, and the difference was statistically significant (p<0.05). Compared with patients with a low level of LINC01857, the rate of lymph node and distant metastasis in patients with a high level of LINC01857 was remarkably higher, while the overall survival rate was lower (p<0.05). In vitro experiments showed that LINC01857 knockdown remarkably decreased the invasion, migration, and crawling ability of GCa cells (p<0.05). Subsequent qRT-PCR results demonstrated that the level of microRNA-200b was remarkably upregulated after the silence of LINC01857. In addition, the silence of microRNA-200b could reverse the biological function of GCa cells induced by the knockout of LINC01857. LINC01857 was highly expressed in GCa, and was associated with lymph node metastasis, distant metastasis, and poor prognosis of patients with GCa. In addition, LINC01857 enhanced the metastatic ability of GCa cells by regulating microRNA-200b.