Low expression of long noncoding RNA CDKN2B-AS1 in patients with idiopathic pulmonary fibrosis predicts lung cancer by regulating the p53-signaling pathway.

The present study aimed to investigate the expression of long non-coding RNA (lncRNA) cyclin dependent kinase inhibitor-2B-antisense RNA 1 CDKN2B-AS1 in patients with peripheral blood of idiopathic pulmonary fibrosis (IPF). A total of 24 patients with IPF and 24 healthy controls were included in the study, four patients with IPF and four healthy controls were selected randomly to extract RNA. There were no other diseases such as hypertension and diabetes in the two groups. RNA from peripheral blood was extracted by high-throughput sequencing and bioinformatics analysis was performed. Based on selected differentially expressed lncRNA and mRNA, gene ontology analysis was performed to screen out the tumor-associated mRNA. A total of 20 samples were chosen to avoid variance due to individual differences. A total of 20 patients with IPF, and 20 controls were further studied, RNA extracted from peripheral blood was used to verify the lncRNA and mRNA levels. A total of 440 lncRNAs were identified to be upregulated and 1,376 downregulated according to the screening results of differential expression. High-throughput sequencing and bioinformatics analysis demonstrated that the expression of CDKN2B-AS1 decreased significantly in patients with IPF compared with healthy controls. The adjacent gene mRNA of CDKN2B-AS1 was identified as CDKN2A, an important anti-oncogene, which is concentrated on the p53 signaling-pathway according to the Kyoto Encyclopedia of Genes and Genomes database. CDKN2A mRNA expression levels were lower in patients with IPF and higher in the control group. The expression of CDKN2B-AS1 and CDKN2A mRNA was significantly lower in IPF group compared with in the control group (P<0.05). The results suggest the expression of the CDKN2B-AS1 and adjacent gene, CDKN2A, are downregulated in the peripheral blood of patients with IPF, which activates the p53-signaling pathway to promote lung cancer formation.