Abstract
Long noncoding RNAs (lncRNAs) play critical roles in carcinoma occurrence and metastasis. LINC00941 has been found to mediate the development of gastric cancer, and LINC00941 was negatively associated with the longer overall survival of lung adenocarcinoma patients. Herein, our aim was to investigate the effects and mechanisms of LINC00941 in NSCLC progression. Microarray was used to identify the change lncRNAs in NSCLC, LINC00941 was found to increase in tumor tissues and patients’ plasma. Knockdown of LINC00941 didn’t modulate the proliferation of NSCLC cells, but inhibition of LINC00941 in NSCLC cells suppressed the angiogenesis ability of human umbilical vein endothelial cells (HUVECs). Moreover, LINC00941 promoted tumorigenesis in vivo, while si-LINC00941 inhibited tumor development of NSCLC. VEGFA was should to be significantly modulated by LINC00941 in NSCLC cells, then luciferase assay proved that LINC00941 regulated VEGFA expression via interacting with miR-877-3p. Followed functional experiments indicated that overexpression of LINC00941 accelerated angiogenesis and NSCLC tumor progression via miR-877-3p/VEGFA axis both in vitro and in vivo. In conclusion, our results clarified the LINC00941 function for the first time, and LINC00941 promoted the progression of NSCLC, which was mediated by miR-877-3p/VEGFA axis. This study might provide new understanding and targets for NSCLC diagnosis and treatment.
Highlights
Lung cancer is the malignant tumor with the highest morbidity and mortality in the world, including non-small cell lung cancer (NSCLC) and small cell lung cancer, of which NSCLC accounts for about 85% [1]
LINC00941 promoted the progression of NSCLC via modulating angiogenesis, which might provide potential biomarkers and novel insight for NSCLC treatment
Bioinformatic analysis was performed to identify the differentially expressed Long noncoding RNAs (lncRNAs) in normal and cancer tissues of NSCLC, which showed an increase of LINC00941 in NSCLC tissues (Figure 1A)
Summary
Lung cancer is the malignant tumor with the highest morbidity and mortality in the world, including non-small cell lung cancer (NSCLC) and small cell lung cancer, of which NSCLC accounts for about 85% [1]. The use of EGFR-TKIs has dramatically improved the clinical efficacy of NSCLC patients, those who are sensitive to treatment will inevitably acquire drug resistance after 10-16 months of treatment, resulting in disease progression five-year survival rate is only 15.9% [3]. Long non-coding RNA (lncRNA) can regulate multiple signal pathways and affect the occurrence and development of NSCLC. Pan et al found that the expression of lncRNA NEAT1 in NSCLC tissues was significantly higher than that in paracancerous tissues, and it was positively correlated with age, vascular invasion, lymph node metastasis, and (TNM) stage of tumor lymph node metastasis [4]. Wang et al found that MEG3 increased the sensitivity of NSCLC to cisplatin by regulating miR-21-5p/SOX7 pathway [5]. The expression of MEG3 is directly regulated by miR-21-5p, miR-21-5p inhibits the effect of MEG3 on cisplatin resistance, SOX7 is the downstream target of miR-21-5p, and MEG3 regulates the expression of SOX7 by inhibiting miR-21-5p [5]
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