Long noncoding RNA, long intergenic non-protein-coding RNA p53-induced transcript (LINC-PINT) was showed to be involved in cancer development. However, the biological effect of LINC-PINT on non-small cell lung cancer (NSCLC) remains unknown. Here, we aimed to investigate the role and underlying mechanism of LINC-PINT in NSCLC. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the level of LINC-PINT in NSCLC tissues and cell lines. Cell counting kit-8 (CCK-8), flow cytometry, migration and transwell invasion assays were used to investigate cell proliferation, cell cycle, cell migration and invasion, respectively. The targets of LINC-PINT were verified by both luciferase reporter assay and RNA immunoprecipitation assay. Tumour xenografts were used to reveal the effect of LINC-PINT on tumourigenesis in vivo. We observed that LINC-PINT expression increased in both NSCLC tissues and cell lines. Function assays exhibited that LINC-PINT reduced NSCLC cell proliferation, cell cycle, cell migration and invasion in vitro. We also indicated that LINC-PINT mediated inhibitory effect on cell proliferation, cell cycle, cell migration and invasion by miR-208a-3p/programmed cell death 4 (PDCD4) in NSCLC cells. These findings indicated that LINC-PINT functions as a tumour-suppressor that exerts important regulatory roles in NSCLC progression by sponging miR-208a-3p/PDCD4.

Long noncoding RNA (lncRNA), specifically the upregulation of lncRNA NR2F1 antisense RNA 1 (NR2F1-AS1), has been involved in the progression of non-small cell lung cancer (NSCLC), but the mechanisms that underlie this remain unclear. In this study, the expression of NR2F1-AS1, miR-363-3p, and SOX4 was assessed in NSCLC cells. A loss-of-function assay was used to measure the tumorigenicity of NSCLC cells. The glycolysis and glutamine metabolism of NSCLC cells was also measured via extracellular acidification rate, consumption of glucose and glutamine, and production of lactate and ATP. The relationships among NR2F1-AS1, miR-363-3p, and SOX4 were detected via dual-luciferase reporter assay. HK-2, GLS1, and SOX4 levels were also analyzed. We found that both NSCLC tissues and cells had higher levels of NR2F1-AS1. Silencing of NR2F1-AS1 inhibited the tumorigenicity of cells in vitro and reduced the glycolysis and glutamine metabolism of NSCLC cells. Regarding its mechanism, NR2F1-AS1 positively regulated the SOX4 level by sponging miR-363-3p. Furthermore, miR-363-3p inhibition or SOX4 overexpression reversed the repressing role of sh-NR2F1-AS1 in the tumorigenicity of NSCLC cells. In summary, NR2F1-AS1 promotes the tumorigenicity of NSCLC cells by regulating miR-363-3p/SOX4.

Some studies have suggested heterogeneous nuclear ribonucleoprotein A2/B1 (HNRNPA2B1) to be a promoter in cancer development. Nonetheless, no detailed pan-cancer investigation has been reported. Thus, this study explored the possible oncogenic role of HNRNPA2B1, such as its expression levels, gene alteration, protein–protein interaction network, immune infiltration, and prognostic value in different cancer types using The Cancer Genome Atlas web platform. Many types of cancer exhibit HNRNPA2B1 overexpression, which is notably associated with poor prognosis. We also found that HNRNPA2B1 with different methylation levels causes a varied prognosis in lung adenocarcinoma (LUAD). It is noteworthy that HNRNPA2B1 levels are connected with cancer-associated fibroblasts in cancers, such as adrenocortical carcinoma, LUAD, and stomach adenocarcinoma. In addition, HNRNPA2B1 participates in the spliceosome- and cell cycle-associated pathways. Finally, HNRNPA2B1 is highly valued in the diagnosis of LUAD, lung squamous cell carcinoma, breast invasive carcinoma, esophageal carcinoma, and liver hepatocellular carcinoma. This systematic study highlighted the role of HNRNPA2B1 in pan-cancer progression.