LINC00261 inhibits progression of pancreatic cancer by down-regulating miR-23a-3p

Abstract

Long noncoding RNAs (lncRNAs) are usually dysregulated in the progression of pancreatic cancer. This research aims to explore the function and mechanism of LINC00261 in pancreatic cancer cell viability, invasion and apoptosis. Cancer Genome Atlas (TCGA) database was applied to analyze the association between survival probability of patients and level of LINC00261 or miR-23a-3p in pancreatic cancer. Quantitative reverse transcription polymerase chain reaction was conducted to analyze the levels of LINC00261 and miR-23a-3p. Cell viability, invasion and apoptosis of pancreatic cancer cells were determined via MTT, transwell invasion assay, and flow cytometry, respectively. The target relationship between LINC00261 and miR-23a-3p was determined via dual-luciferase reporter and RNA immunoprecipitation assays. Low level of LINC00261 indicated low survival probability of pancreatic cancer patients. LINC00261 level was decreased in pancreatic cancer cells than that in normal pancreatic ductal epithelial cells. Addition of LINC00261 restrained cell viability and invasion and facilitated apoptosis. miR-23a-3p was negatively correlated with LINC00261 level and high expression of miR-23a-3p indicated low survival probability. miR-23a-3p was targeted by LINC00261 and attenuated the influence of LINC00261 on pancreatic cancer cell viability, invasion and apoptosis. In conclusion, LINC00261 overexpression repressed cell viability and invasion and enhanced apoptosis by decreasing miR-23a-3p expression in pancreatic cancer cells, indicating a new target for the treatment of pancreatic cancer.

Keywords: Apoptosis; Invasion; LINC00261; Pancreatic cancer; Viability; miR-23a-3p.