Abstract
BACKGROUND: In recent years, long noncoding RNAs (lncRNAs) relate to many biological processes, which affect the progression of tumors. Transient receptor potential melastatin 2 antisense RNA (TRPM2-AS) is reported to play an oncogene-like role in tumors. TRPM2-AS is highly expressed in colorectal cancer (CRC), but the mechanism of TRPM2-AS is still unclear. The regulatory mechanism of TRPM2-AS in the occurrence of CRC was explored, so as to find new markers and therapeutic targets for CRC. METHODS: TRPM2-AS and miR-22-3p expression in CRC cells were measured through reverse-transcription quantitative polymerase chain reaction (RT-qPCR). Then, TRPM2-AS knockdown cell lines were constructed, and cell counting kit-8 (CCK-8), clone formation, wound healing, and invasion assays were used to detect cell malignant behavior. Follistatin-like 1 (FSTL1) protein was detected by western blotting. The interaction between miR-22-3p and TRPM2-AS or FSTL1 was verified by the luciferase reporter and RNA immunoprecipitation (RIP) assay. Subcutaneous xenografts were performed using animal experiments. RESULTS: TRPM2-AS expression in CRC cells was increased, and miR-22-3p expression was decreased in CRC cells. TRPM2-AS inhibition inhibited cell malignant behavior. miR-22-3p has a targeting relationship with TRPM2-AS and FSTL1. In cells, downregulation of TRPM2-AS expression promoted miR-22-3p and inhibited FSTL1 expression, while mimics inhibited FSTL1 expression. miR-22-3p inhibition or FSTL1 overexpression could offset the inhibition of TRPM2-AS downregulation on CRC cells. CONCLUSIONS: The TRPM2-AS/miR-22-3p/FSTL1 regulation axis could regulate CRC cell malignant behavior, which may provide a new perspective for interpreting the mechanism of CRC development.