Abstract
Long noncoding RNAs (lncRNAs) have emerged as regulators of gene expression and play critical regulatory roles in diverse biological functions and diseases, including cancer. In this study, we report the downregulation of LINC01089 in non-small cell lung cancer (NSCLC) samples, relative to adjacent non-tumor tissues, and demonstrate its role in the inhibition of proliferation, migration, and epithelial–mesenchymal transition (EMT) of NSCLC cells. Mechanistic analysis indicates that LINC01089 acts as a sponge for miR-27a, regulating its expression in NSCLC. Interestingly, LINC01089 mediated the upregulation of SFRP1 expression by inhibiting the Wnt/β-catenin–EMT pathway and inhibiting the epithelial–mesenchymal transition of NSCLC via sponging miR-27a. Overall, our findings highlight LINC01089’s tumorigenic role and regulatory mechanism in NSCLC, thereby suggesting its potential as a therapeutic target for managing NSCLC.
Highlights
Lung cancer is one of the most commonly diagnosed cancers in both sexes, accounting for 11.6 and 18.4% of all cancer cases and cancer-related deaths, respectively, worldwide [1]
A search on the Gene Expression Profiling Interactive Analysis (GEPIA) database revealed a downregulation of LINC01089 expression in both lung adenocarcinoma and lung squamous carcinoma samples, relative to the adjacent normal tissues (Figure S1A, Figure S1B)
The 60 Non-small cell lung cancer (NSCLC) patients enrolled in our study revealed two groups based on the median level of LINC01089 expression in NSCLC tissues
Summary
Lung cancer is one of the most commonly diagnosed cancers in both sexes, accounting for 11.6 and 18.4% of all cancer cases and cancer-related deaths, respectively, worldwide [1]. Previous studies have shown that lncRNAs are involved in fundamental biological mechanisms, with a close association to the occurrence of several cancer types, including lung cancer [4], gastric carcinoma [5], prostate cancer [6, 7], and hepatocellular carcinoma [8, 9] among others. Despite their potential as therapeutic targets for cancer treatment, a detailed description of the underlying molecular mechanisms of lncRNAs, especially in NSCLC, remains unclear
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