NEAT1/hsa‐mir‐98‐5p/MAPK6 axis is involved in non–small‐cell lung cancer development

Long noncoding RNAs (lncRNAs) or microRNAs belong to the two most important noncoding RNAs and they are involved in a lot of cancers, including non–small‐cell lung cancer (NSCLC). Therefore, currently, we focused on the biological and clinical significance of lncRNA nuclear enriched abundant transcript 1 (NEAT1) and hsa‐mir‐98‐5p in NSCLC. It was observed that NEAT1 was upregulated while hsa‐mir‐98‐5p was downregulated respectively in NSCLC cell lines compared to human normal lung epithelial BES‐2B cells. Inhibition of NEAT1 can suppress the progression of NSCLC cells and hsa‐mir‐98‐5p can reverse this phenomenon. Bioinformatics search was used to elucidate the correlation between NEAT1 and hsa‐mir‐98‐5p. Additionally, a novel messenger RNA target of hsa‐mir‐98‐5p, mitogen‐activated protein kinase 6 (MAPK6), was predicted. Overexpression and knockdown studies were conducted to verify whether NEAT1 exhibits its biological functions through regulating hsa‐mir‐98‐5p and MAPK6 in vitro. NEAT1 was able to increase MAPK6 expression and hsa‐mir‐98‐5p mimics can inhibit MAPK6 via downregulating NEAT1 levels. We speculated that NEAT1 may act as a competing endogenous lncRNA to upregulate MAPK6 by attaching hsa‐mir‐98‐5p in lung cancers. Taken these together, NEAT1/hsa‐mir‐98‐5p/MAPK6 is involved in the development and progress in NSCLC. NEAT1 could be recommended as a prognostic biomarker and therapeutic indicator in NSCLC diagnosis and treatment. Our study is the first reporting of a possible mechanism for a crosstalk between nuclear enriched abundant transcript 1 (NEAT1) and hsa‐mir‐98‐5p crosstalk in non–small‐cell lung cancer inhibition. We showed NEAT1/hsa‐mir‐98‐5p/MAPK6 plays a critical role in the growth, migration, and invasion of lung cancer cells.