LncRNA SLC12A9-AS1 Drives Malignant Progression in Colorectal Cancer by Regulating miR-139-3p.

Abstract

This study investigated the function of long noncoding RNA SLC12A9-AS1 in colorectal cancer (CRC) cells and its potential regulatory mechanism. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure SLC12A9-AS1 and miR-139-3p expression in CRC cell lines. Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay, whereas migration and invasion were evaluated using permeable cell culture insert assays. The interaction between SLC12A9-AS1 and miR-139-3p was examined using dual-luciferase reporter (DLR) and RNA immunoprecipitation (RIP) assays. SLC12A9-AS1 was significantly upregulated, whereas miR-139-3p was downregulated, in CRC cells. Silencing SLC12A9-AS1 markedly reduced cell viability, migration, invasion, and epithelial-mesenchymal transition (EMT). The DLR and RIP assays supported an interaction between SLC12A9-AS1 and miR-139-3p. In addition, inhibition of miR-139-3p reversed the suppressive effects of SLC12A9-AS1 knockdown on malignant cellular phenotypes. Collectively, these findings indicate that SLC12A9-AS1 is abnormally overexpressed in CRC cells and that its knockdown attenuates malignant phenotypes, at least in part through regulation of miR-139-3p. These results provide new in vitro experimental evidence for understanding the molecular mechanisms involved in CRC pathogenesis.