lncRNA FLVCR1‑AS1 drives colorectal cancer progression via modulation of the miR‑381/RAP2A axis.

Colorectal cancer (CRC) is one of the most prevalent types of cancer globally. Long non‑coding RNAs (lncRNAs) have been suggested to serve as vital regulators in CRC. lncRNA feline leukemia virus subgroup C receptor 1 antisense RNA 1 (FLVCR1‑AS1) is closely associated with the tumorigenesis of various types of cancer. The aim of the present study was to investigate the molecular mechanisms of lncRNA FLVCR1‑AS1 in CRC progression. The expression levels of FLVCR1‑AS1, microRNA (miR)‑381 and Ras‑related protein 2a (RAP2A) were measured by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). A Kaplan‑Meier analysis was performed to determine the overall survival rate of patients with CRC. Furthermore, cell viability, migration and invasion were assessed using Cell Counting Kit‑8 (CCK‑8) and Transwell assays. The interaction between genes was confirmed using dual‑luciferase reporter and pull‑down assays. The results demonstrated that FLVCR1‑AS1 was upregulated in CRC tissues and cells, and increased FLVCR1‑AS1 expression levels in patients with CRC were associated with poor prognosis. FLVCR1‑AS1 knockdown significantly attenuated the viability, migration and invasion ability of CRC cells. In addition, the results confirmed that FLVCR1‑AS1 directly binds with miR‑381‑3p, and that RAP2A is a direct target of miR‑381‑3p. The overexpression of FLVCR1‑AS1 increased RAP2A expression levels. Functional assays revealed that miR‑381 inhibitor or RAP2A overexpression attenuated the suppressive effects of FLVCR1‑AS1 silencing on CRC cell viability, migration and invasion. Overall, the findings of the current study suggest that FLVCR1‑AS1 promotes CRC progression via the miR‑381/RAP2A pathway. These findings may provide a novel approach for CRC treatment.