Abstract
Long non‑coding RNA (lncRNA) actin filament‑associated protein 1 antisense RNA 1 (AFAP1‑AS1) has been reported to serve important roles in multiple types of cancer. However, the biological function and underlying mechanism of AFAP1‑AS1 in oral squamous cell carcinoma (OSCC) remain largely unknown. The present study aimed to investigate the biological roles and clarify the potential mechanism of AFAP1‑AS1 in OSCC. The expression levels of AFAP1‑AS1 in OSCC tissues and cells were determined using reverse transcription‑quantitative PCR. Cell proliferation, colony formation, migration and invasion were analyzed using Cell Counting Kit‑8, colony formation, wound healing and Transwell invasion assays, respectively. The potential binding between AFAP1‑AS1 and microRNA (miR)‑145 was validated using dual luciferase reporter and RNA pull‑down assays. A xenograft tumor model was established to evaluate the effect of AFAP1‑AS1 in vivo. The results revealed that AFAP1‑AS1 expression levels were markedly upregulated in OSCC tissues and cells. In addition, patients with OSCC with high expression levels of AFAP1‑AS1 had a poor prognosis. Functionally, the knockdown of AFAP1‑AS1 in OSCC cells significantly inhibited cell proliferation, migration and invasion in vitro. Similarly, in vivo AFAP1‑AS1 knockdown prevented tumor growth and reduced tumor size and weight. Mechanistically, AFAP1‑AS1 was discovered to regulate the expression levels of Homeobox A1 (HOXA1) by competing with miR‑145. The inhibition of miR‑145 partially attenuated the inhibitory effects of AFAP1‑AS1 knockdown on OSCC cells. In conclusion, the findings of the present study suggested that AFAP1‑AS1 may promote the progression of OSCC by regulating the miR‑145/HOXA1 axis.