Abstract
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. 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. 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. 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.
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