Long Noncoding RNA SNHG6 Promotes Proliferation and Inhibits Apoptosis in Non-small Cell Lung Cancer Cells by Regulating miR-490-3p/RSF1 Axis

被引:27
作者
Dong, Zheng [1 ]
Liu, Honglai [2 ]
Zhao, Guangli [3 ]
机构
[1] Linyi Cent Hosp, Dept Resp Med, Linyi, Shandong, Peoples R China
[2] Yishui Cty Peoples Hosp, Dept Thorac Surg, Linyi, Shandong, Peoples R China
[3] Lanling Peoples Hosp, Dept Oncol, Linyi, Shandong, Peoples R China
关键词
SNHG6; miR-490-3p; RSF1; progression; NSCLC; LNCRNA SNHG6; MESENCHYMAL TRANSITION; SIGNALING PATHWAY; POOR-PROGNOSIS; UP-REGULATION; INVASION; MIGRATION; EXPRESSION; CARCINOMA; GROWTH;
D O I
10.1089/cbr.2019.3120
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background:Nonsmall cell lung cancer (NSCLC) is a malignant cancer type and has developed into the leading cause of cancer-related death worldwide. Small nucleolar RNA host gene 6 (SNHG6) has been identified as an oncogene in multiple cancers. However, the functions of SNHG6 in tumorigenesis and progression of NSCLC are still poorly understood. Materials and Methods:The expression of SNHG6, miR-490-3p, and remodeling and spacing factor 1 (RSF1) in NSCLC tumors and cells was measured by quantitative real-time polymerase chain reaction. The correlation between miR-490-3p and SNHG6 or RSF1 was analyzed by Pearson's correlation coefficient. Luciferase reporter assay was employed for verifying the interaction between miR-490-3p and SNHG6 or RSF1. Cell viability was examined by 3-(4, 5)-dimethylthiazole-2-y1)-2, 5-biphenyl tetrazolium bromide (MTT) assay. Cell apoptosis was evaluated by flow cytometry and Western blot, respectively. Protein expression of RSF1, Bcl-2, Bax, and cleaved caspase-3 (cleaved casp-3) was detected by Western blot assay. Xenograft mice models were established by subcutaneously injecting H460 cells stably transfected with sh-SNHG6 and sh-NC. Results:SNHG6 and RSF1 expression were upregulated, whereas miR-490-3p was downregulated in NSCLC tumors and cell lines compared with normal tissues and cells. Pearson's correlation coefficient analysis indicated that miR-490-3p was correlated with SNHG6 and RSF1 inversely. Then, luciferase reporter assay confirmed the interaction between miR-490-3p and SNHG6 or RSF1. More importantly, the rescue experiments clarified that miR-490-3p inhibitor could relieve SNHG6 silencing-mediated inhibition on proliferation and promotion on apoptosis in NSCLC. In addition, the authors discovered that SNHG6 promoted cell progression by regulating miR-490-3p/RSF1 axis. However, SNHG6 knockdown hindered tumor growthin vivoby regulating RSF1 by targeting miR-490-3p. Conclusion:The authors demonstrated that SNHG6 promoted proliferation and inhibits apoptosis in NSCLC by regulating miR-490-3p/RSF1 axis, representing promising targeted therapeutic strategies against NSCLC.
引用
收藏
页码:351 / 361
页数:11
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