Silencing of LncRNA AFAP1-AS1 Inhibits Cell Proliferation in Oral Squamous Cancer by Suppressing CCNA2.

BACKGROUND

Evidence has indicated that dysregulation of long noncoding RNAs (lncRNA) is a critical factor in the occurrence of many diseases, including cancer. The lncRNA AFAP1-AS1 has been shown to participate in oncogenesis, metastasis, or drug resistance in many types of cancer. However, the potential role of AFAP1-AS1 in oral squamous cell carcinoma (OSCC) has not been fully elucidated.

METHODS

Bioinformatics analysis was performed to compare AFAP1-AS1 expression levels in OSCC cancer samples and in normal controls. The biological function of AFAP1-AS1 was studied through loss-of-function assays. To study the potential mechanisms, high-throughput sequencing was applied to OSCC cancer samples and a series of bioinformatics analyses were performed. The effects of AFAP1-AS1 on OSCC tumor growth was evaluated by in vivo xenograft tumor formation assays.

RESULTS

Bioinformatics analyses indicated that AFAP1-AS1 was upregulated in OSCC. Overexpression of AFAP1-AS1 was positively correlated with lymph node metastasis, tumor stage, and pathological grade. Down-regulation of AFAP1-AS1 in OSCC led to decreased proliferation in vitro and, notably, inhibition of tumor growth in vivo. Further research indicated that AFAP1-AS1 regulated OSCC cell proliferation by targeting CCNA2.

CONCLUSION

AFAP1-AS1 promotes tumor proliferation and indicates a poor prognosis in OSCC, providing a potential therapeutic strategy.