lncRNA FLVCR1­AS1 drives colorectal cancer progression via modulation of the miR­381/RAP2A axis.

ABSTRACT

Colorectal cancer (CRC) is one of the most prevalent types of cancer globally. Long non­coding RNAs (lncRNAs) have been suggested to serve as vital regulators in CRC. lncRNA feline leukemia virus subgroup C receptor 1 antisense RNA 1 (FLVCR1­AS1) 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 FLVCR1­AS1 in CRC progression. The expression levels of FLVCR1­AS1, microRNA (miR)­381 and Ras­related protein 2a (RAP2A) were measured by reverse transcription­quantitative polymerase chain reaction (RT­qPCR). A Kaplan­Meier analysis was performed to determine the overall survival rate of patients with CRC. Furthermore, cell viability, migration and invasion were assessed using Cell Counting Kit­8 (CCK­8) and Transwell assays. The interaction between genes was confirmed using dual­luciferase reporter and pull­down assays. The results demonstrated that FLVCR1­AS1 was upregulated in CRC tissues and cells, and increased FLVCR1­AS1 expression levels in patients with CRC were associated with poor prognosis. FLVCR1­AS1 knockdown significantly attenuated the viability, migration and invasion ability of CRC cells. In addition, the results confirmed that FLVCR1­AS1 directly binds with miR­381­3p, and that RAP2A is a direct target of miR­381­3p. The overexpression of FLVCR1­AS1 increased RAP2A expression levels. Functional assays revealed that miR­381 inhibitor or RAP2A overexpression attenuated the suppressive effects of FLVCR1­AS1 silencing on CRC cell viability, migration and invasion. Overall, the findings of the current study suggest that FLVCR1­AS1 promotes CRC progression via the miR­381/RAP2A pathway. These findings may provide a novel approach for CRC treatment.