Abstract
Background: Long non-coding RNAs (lncRNAs) have been consistently reported to be involved in the progression of non-small cell lung cancer (NSCLC). In this study, we aimed to identify aberrantly expressed lncRNAs in NSCLC, in order to explore new therapeutic targets for NSCLC.Methods: Two pairs of NSCLC and adjacent normal tissues were first analyzed by RNA sequencing. The expressions of LINC00702 in 40 pairs patient samples and in 4 NSCLC cell lines was measured by quantitative real-time PCR. Putative target miRNAs of LINC00702 were predicted by the bioinformatics tools. The effect of LINC00702 on tumor growth in vivo was evaluated.Results: LINC00702 was significantly down-regulated in patients with NSCLC, which was correlated with tumor size and metastasis. In addition, overexpression of LINC00702 markedly suppressed proliferation and metastasis in NSCLC cells via inducing apoptosis in vitro and in vivo. Moreover, bioinformatics and luciferase reporter assays demonstrated that LINC00702 functioned as a competing endogenous RNA (ceRNA) for miR-510 in NSCLC, and upregulated its target gene PTEN.Conclusion: Our results indicated that LINC00702 modulated the expression of PTEN gene by acting as a ceRNA for miR-510 in NSCLC. Therefore, LINC00702 may serve as a potential target for the diagnosis and treatment of patients with NSCLC.
Highlights
Lung cancer is the leading cause of cancer-related mortality worldwide
Differential expressed genes were analyzed using clustering analysis which were marked in red (Figure. 1A, 1B). 74 upregulated Long non-coding RNAs (lncRNAs) and 1 downregulated lncRNAs were observed between non-small cell lung cancer (NSCLC) and adjacent tissues (Figure 1C)
Differential expressed genes (DEGs) between NSCLC and adjacent tissues were recorded in Volcano plot with the criteria of false discovery rate (FDR) < 0.01 or log2 fold-change (FC) ≥ 4, which were marked in yellow (Figure. 1C)
Summary
Lung cancer is the leading cause of cancer-related mortality worldwide. Non-small cell lung cancer (NSCLC) accounts for about 80% of all lung cancer cases and about 75% of the patients are diagnosed in the advanced stages of the disease, with a 5-year overall survival rate < 15% [1]. In order to identify new therapeutic targets and improve clinical outcome of patients, the molecular basis for NSCLC needs to be elucidated. Studies have found that several lncRNAs are abnormally expressed in lung cancer tissues, which are associated with tumor invasion, metastasis and prognosis [2, 3]. Long non-coding RNAs (lncRNAs) have been consistently reported to be involved in the progression of non-small cell lung cancer (NSCLC). We aimed to identify aberrantly expressed lncRNAs in NSCLC, in order to explore new therapeutic targets for NSCLC. Results: LINC00702 was significantly down-regulated in patients with NSCLC, which was correlated with tumor size and metastasis. Bioinformatics and luciferase reporter assays demonstrated that LINC00702 functioned as a competing endogenous RNA (ceRNA) for miR-510 in NSCLC, and upregulated its target gene PTEN. LINC00702 may serve as a potential target for the diagnosis and treatment of patients with NSCLC
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