Long non‐coding RNA AGAP2‐AS1 accelerates cell proliferation, migration, invasion and the EMT process in colorectal cancer via regulating the miR‐4,668‐3p/SRSF1 axis

Background Colorectal cancer (CRC) is a frequently occurring tumor. Although a number of long noncoding RNAs have been researched in CRC, the expression, function and mechanism of AGAP2‐AS1 remains poorly investigated. Methods Gene expression was analyzed by a quantitative reverse transcriptase‐polymerase chain rreaction and western blot analyses. Cell counting kit‐8, colony formation and Transwell assays were utilized to explore the functional role of AGAP2‐AS1 in CRC. Luciferase reporter, RNA pull down and RNA immunoprecipitation assays were implemented to verify relationships between RNA molecules. Results In the present study, AGAP2‐AS1 was unveiled as highly expressed in CRC cell lines compared to normal cells. AGAP2‐AS1 knockdown suppressed cell proliferation, migration, invasion and the epithelial‐to‐mesenchymal transition process. Interestingly, AGAP2‐AS1 sponges miR‐4,668‐3p to release SRSF1 in CRC. Furthermore, in the rescue functional assay, miR‐4,668‐3p down‐regulation exacerbated the malignant behaviors of AGAP2‐AS1‐depleted CRC cells, whereas such effects were further offset by SRSF1 knockdown. Conclusions AGAP2‐AS1 facilitates cell proliferation, motility and EMT in CRC via targeting the miR‐4,668‐3p/SRSF1 axis. AGAP2‐AS1 or SRSF1 may have potential as underlying therapeutic targets for CRC patients. In CRC cells, AGAP2‐AS1 protects SRSF1 mRNA from miR‐4668‐3p‐induced silencing through competitively interacting with miR‐4668‐3p, enhancing SRSF1 expression to facilitate cell proliferation, migration, invasion and EMT process.