Abstract
BackgroundlncRNAs and VEGF have been shown to have close connections with oral squamous cell carcinoma (OSCC). We explored the interaction between lncRNA NEAT1 and VEGF-A in OSCC.MethodsRT-qPCR was implemented to measure levels of lncRNA NEAT1 and VEGF-A in OSCC cell lines and normal cell lines. Cell functions then were checked after regulating the expressions of lncRNA NEAT1 and VEGF-A separately. Cell viabilities were examined with CCK-8 and apoptosis rate was checked with flow cytometry. Meanwhile, EMT-related genes E-cadherin, N-cadherin, Vimentin, and Snail and Notch signaling genes Notch1, Notch2, and Jagged were evaluated by RT-qPCR. IMR-1 was applied for impeding Notch signaling pathway. Later, cell viabilities, apoptosis, and EMT were assessed.ResultsExpressions of lncRNA NEAT1 and VEGF-A were both increased significantly in OSCC cell lines especially in TSCC1 cell line. Suppression of lncNRA NEAT1 was associated with lower cell viabilities and EMT and higher apoptosis rate in the TSCC1 cell line. Meanwhile, knockdown of VEGF-A significantly repressed cell viabilities and EMT in the TSCC1 cell line. Magnifying functions of inhibited lncRNA NEAT1 Notch signaling pathway was obviously activated with overexpressions of lncRNA NEAT1 and VEGF-A. Adding IMR-1 significantly downregulated cell viabilities and EMT and sharply increased apoptosis in the context of lncRNA NEAT1 and VEGF-A overexpression.ConclusionLncRNA NEAT1 may upregulate proliferation and EMT and repress apoptosis through activating VEGF-A and Notch signaling pathway in vitro, suggesting an underlying regulatory factor in OSCC. Nevertheless, further research is necessary to gain a greater understanding of lncRNA NEAT1 and connections with VEGF-A in vivo and in clinical study.
Highlights
Oral squamous cell carcinoma (OSCC) is a head and neck malignant cancer with high aggressiveness that can invade adjacent bones, muscles, skin tissues, and local lymphoid tissues [1, 2], which takes up about 3% among all kinds of new cases of malignancies [3]
LncRNA Nuclear paraspeckle assembly transcript 1 (NEAT1) was highly expressed in oral squamous cell carcinoma (OSCC) cell lines and accelerated proliferation and Epithelial-tomesenchymal transition (EMT) but suppressed apoptosis in OSCC cells According to results of RT-qPCR, expressions of lncRNA NEAT1 expressed significantly higher in OSCC cell lines than in normal HOEC cell line
As lncRNA NEAT1 was highly expressed in OSCC cancer cells, two kinds of siRNAs were used to knock down lncRNA NEAT1 in cells
Summary
Oral squamous cell carcinoma (OSCC) is a head and neck malignant cancer with high aggressiveness that can invade adjacent bones, muscles, skin tissues, and local lymphoid tissues [1, 2], which takes up about 3% among all kinds of new cases of malignancies [3]. Though surgery and chemoradiotherapy techniques have made progress, the 5-year overall survival rate of OSCC is only 40–60% [4,5,6]. It is necessary to dig out the nosogenesis of OSCC and mechanisms that can regulate progression of OSCC in order to reduce its morbidity and increase cure and survival rate of patients. LncRNAs and VEGF have been shown to have close connections with oral squamous cell carcinoma (OSCC). We explored the interaction between lncRNA NEAT1 and VEGF-A in OSCC
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