Long noncoding RNA AFAP1-AS1 promotes osteosarcoma progression by regulating miR-497/IGF1R axis.

Long non-coding RNA (lncRNA) actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) has been reported to be involved in the progression of multiple cancers. However, exact function and regulatory mechanism of AFAP1-AS1 in osteosarcoma (OS) remain largely unclear. In this study, quantitative real time polymerase chain reaction (qRT-PCR) revealed that AFAP1-AS1 was upregulated in OS tissues and cell lines. Increased AFAP1-AS1 was associated with poor prognosis. Loss-of-function experiments demonstrated that knockdown of AFAP1-AS1 inhibited the proliferation, colony formation, migration, invasion and induced cell apoptosis. Bioinformatics analysis and luciferase reporter assays confirmed that mircoRNA-497 (miR-497) was a directly target of AFAP1-AS1. Rescue experiments confirmed that miR-497 inhibition could partially reverse the inhibitory effect of AFAP1-AS1 knockdown on OS cells. Moreover, AFAP1-AS1 modulated the expression of insulin-like growth factor 1 receptor (IGF1R, a target of miR-497) indirectly. In vivo xenograft tumor assay showed that AFAP1-AS1 knockdown inhibited tumor tumorigenesis. Taken together, these findings indicate that AFAP1-AS1 promotes OS progression by regulating miR-497/IGF1R axis, providing a therapeutic target for OS.