ABSTRACT
Non-coding RNAs (ncRNAs) have been demonstrated to modulate the oncogenesis of non-small cell lung cancer (NSCLC), especially the long non-coding RNAs (lncRNAs). However, the role of lncRNA FOXC2-AS1 in the NSCLC is still unclear. In this research, we find that lncRNA FOXC2-AS1 is involved to NSCLC oncogenesis. The ectopic high-expression level of FOXC2-AS1 is closely correlated with the limited NSCLC patients' survival. In the functional experiments, the knockdown of FOXC2-AS1 dramatically suppressed the NSCLC cells' (A549, H460) proliferation, accelerated the apoptosis and induced the cycle arrest at G0/G1 phase. Mechanistic experiments revealed that FOXC2-AS1 repressed the p15 expression via recruiting the polycomb repressive complex 2 (PRC2) to the promoter of p15. The interaction within FOXC2-AS1 and p15 was validated using the rescue experiments. In conclusion, the results in this work confirmed that FOXC2-AS1 could aggravate NSCLC oncogenesis through repressing p15 expression via interacting EZH2, which provide new idea for the NSCLC therapeutic strategy.
