circASS1 overexpression inhibits the proliferation, invasion and migration of colorectal cancer cells by regulating the miR-1269a/VASH1 axis

xlomafota13 shared this article with you from Inoreader circASS1 overexpression inhibits the proliferation, invasion and migration of colorectal cancer cells by regulating the miR-1269a/VASH1 axis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1155. doi: 10.3892/etm.2021.10589. Epub 2021 Aug 10. ABSTRACT Colorectal cancer (CRC), the third most common cancer worldwide, poses a threat to human life. However, its underlying mechanism is unclear and no satisfactory treatment is available. The present study aimed to investigate the role of circular RNA argininosuccinate synthase 1 (circASS1) in CRC cells and tissues to identify the potential mechanism underlying the pathogenesis of CRC. The expression of circASS1 in CRC cells and tissues was determined by reverse transcription-quantitative PCR. Following circASS1 overexpression in HT29 cells, cell viability, colony formation and apoptosis were measured using MTT, colony formation and TUNEL assays, respectively. Cell invasion and migration were also assessed. After confirming the associations among circASS1, microRNA (miR)-1269a and vasohibin 1 (VASH1), the characteristics of the HT29 cell line were as sessed by performing the aforementioned assays. circASS1 expression was decreased in CRC cells and tissues, and circASS1 overexpression suppressed CRC cell proliferation, invasion and migration. circASS1 adsorbed miR-1269a and regulated its expression, and VASH1 was a target protein of miR-1269a. circASS1 overexpression decreased cell proliferation, invasion and migration, but enhanced cell apoptosis in HT29 cells, which was reversed by co-transfection with miR-1269a mimic or short hairpin RNA-VASH1. In conclusion, circASS1 overexpression inhibited CRC cell proliferation, invasion and migration by regulating miR-1269a/VASH1, which indicated a potential molecular mechanism underlying the pathogenesis of CRC. PMID:34504600 | PM C:PMC8393656 | DOI:10.3892/etm.2021.10589 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.