Abstract
The two broad histological subtypes of lung cancer are small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC), which are the leading causes of cancer-related death in the world. Long noncoding RNAs (lncRNAs) have been verified to be critical in the regulation of cancer development. The present study identified and elucidated the regulatory roles of a novel lncRNA MRUL in NSCLC. The results showed that MRUL was overexpressed in NSCLC samples and correlated with the poor prognosis of patients who had NSCLC. Moreover, this research has for the first time demonstrated that MRUL acted as an oncogenetic lncRNA in NSCLC. Knockdown of MRUL considerably repressed NSCLC cell proliferation, invasion, and migration. The bioinformatics analysis showed that MRUL was involved in regulating multiple RNA splicing and proliferation-related biological processes, such as mRNA splicing, RNA splicing, mRNA processing, mRNA 3′-end processing, mRNA splice site selection, and DNA replication. By combining bioinformatics analysis and experimental validation, we found that MRUL regulated NSCLC progression through promoting SRSF2 by sponging miR-17 in NSCLC cells. The discoveries indicated that MRUL could be a therapeutic target and a potential diagnostic for NSCLC.
Highlights
Lung cancer, which includes small cell lung cancer (SCLC) [1] and non-small cell lung cancer (NSCLC) [2], has been playing the leading part in causing tumor-related death worldwide
Emerging evidences demonstrated that Long noncoding RNAs (lncRNAs) were deregulated and played crucial roles in tumor tumorigenesis and pathogenesis
In NSCLC, a series of lncRNAs were reported to be related to cancer progression
Summary
Lung cancer, which includes small cell lung cancer (SCLC) [1] and non-small cell lung cancer (NSCLC) [2], has been playing the leading part in causing tumor-related death worldwide. NSCLC can be classified into subcategories of squamous cell carcinoma, adenocarcinoma, and large cell carcinoma [3]. Multiple causes, such as genetic factors, air pollution, and smoking, were regarded to be related to NSCLC progression. Emerging studies demonstrated that lncRNAs participated in regulating cancer tumorigenesis and progression through multiple cancer-related pathways, including Wnt signaling and PI3K signaling. The contribution to NSCLC’s progression by lncRNA SNHG1 is made by activating Wnt/β-catenin signaling pathway [6] and inhibiting
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