AFAP1-AS1 was the most significantly upregulated lncRNA in lung cancer. Elevated AFAP1-AS1 expression was associated with poor prognosis, suggesting that AFAP1-AS1 may be a useful biomarker for the prediction of lung cancer progression and prognosis.

LncRNA AFAP1-AS1 was up-regulated in non-small lung carcinoma tissues and it could be an independent prognostic indicator.

AFAP1-AS1 expression level was significantly elevated in non-small cell lung cancer patients compared with that in normal controls.

Results showed that expression of the lncRNA AFAP1-AS1 is upregulated in non-small cell lung cancer (NSCLC) tissues and cells, and associated with poor prognosis of NSCLC patients. The loss of AFAP1-AS1 inhibited NSCLC cell proliferation in vitro and suppressed tumor growth in vivo. Furthermore, AFAP1-AS1-mediated oncogenic effects occurred partially through epigenetic suppression of p21 expression by binding to EZH2.

expressions of AFAP1-AS1 were associated with pathological grade, TNM staging and metastatic potential of non-small cell lung cancer. AFAP1-AS1 could activate interferon regulatory factor (IRF)7, the retinoid-inducible protein (RIG)-I-like receptor signaling pathway and Bcl-2 in vitro.

This study demonstrates that AFAP1-AS1 acts as an oncogene in non-small cell lung cancer (NSCLC) to promote cell migration partly by upregulating AFAP1 expression, while its own expression is controlled by DNA methylation, and highlights its diagnostic and therapeutic values for NSCLC patients.

Findings showed that AFAP1-AS1 is upregulated in non-small-cell lung cancer (NSCLC) tissues and cells, and that high AFAP1-AS1 expression in NSCLC patients suggests worse outcomes. Furthermore, AFAP1-AS1 can promote NSCLC cell proliferation and migration through epigenetic silencing of tumor suppressor HBP1.