Objective: To illustrate the role of FOXF2 in the aggravation of the progression of non-small cell lung cancer (NSCLC) by targeting long non-coding RNA (lncRNA) H19 to down-regulate the gene of phosphate and tensin homolog deleted on chromosome ten (PTEN).
Patients and methods: The relative levels of FOXF2 and H19 in NSCLC tissues and adjacent normal tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between the expression levels of FOXF2 and H19 was analyzed. Kaplan-Meier curves were depicted for uncovering the prognostic value of FOXF2 in NSCLC patients. The proliferative and migratory abilities of A549 cells influenced by FOXF2 were also assessed. The interaction between FOXF2 and H19 was evaluated through chromatin immunoprecipitation (ChIP) assay and Western blot, so did the association between H19 and PTEN. Finally, rescue experiments were conducted to explore the role of FOXF2/H19/PTEN axis in regulating the viability and migration of A549 cells.
Results: FOXF2 and H19 were upregulated in NSCLC and a positive correlation was observed between the two genes. High level of FOXF2 indicated a worse prognosis in NSCLC patients. The knockdown of FOXF2 attenuated the proliferative and migratory abilities of A549 cells. FOXF2 could bind to the promoter region of H19 and accelerated its transcription. Moreover, H19 could recruit EZH2 to bind to PTEN. The overexpression of H19 could reverse the regulatory effects of FOXF2 on the viability and migration of A549 cells.
Conclusions: FOXF2 was upregulated in NSCLC. It accelerated the proliferative and migratory abilities of the NSCLC cells by targeting H19 to downregulate PTEN, thus aggravating the progression of NSCLC.