LINC01711 facilitated gastric carcinoma progression by sponging miR-140-3p

Abstract Objectives Gastric carcinoma (GC) remains a high-mortality malignancy that needs efficient ways for the prognosis and therapy of the disease. LncRNAs are biomolecules that participate in cancer progression by regulating gene expression. This study thus investigated the role of lncRNA LINC01711 in GC progression and the underlying mechanisms. Methods GC tumor and normal tissues were collected from 150 GC patients. qRT-PCR was used to test the expression of biomolecules. LncBook, Miranda, and starBase databases were employed to explore miRNAs that interact with LINC01711. The association between the biomolecules was validated via a dual luciferase reporter assay. Biological functions of biomolecules in GC cells were measured by the Cell Counting Kit-8 (CCK-8) and the transwell migration and invasion assays. Results This study found an upregulation of LINC01711 in GC tumor tissues compared to normal tissues. The upregulation of LINC01711 was an indicator of adverse clinical outcomes in GC patients. The miRNA that interacted with LINC01711 in GC was hsa-miR-140-3p. There was a negative correlation between the expression levels of LINC01711 and hsa-miR-140-3p in both GC tumor tissues and cells. LINC01711 promoted GC tumor cell proliferation, migration, and invasion by sponging hsa-miR-140-3p. Conclusions LINC01711 might be an ideal prognostic marker and treatment target for GC. The upregulation of LINC01711 was a negative prognostic indicator for GC patients. LINC01711 facilitated GC tumor cell activities related to GC progression by sponging hsa-miR-140-3p.