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


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



Cancer BioTherapy and Radiopharmaceuticals 35(5): 351-361



ISSN/ISBN: 1084-9785

PMID: 32202941

DOI: 10.1089/cbr.2019.3120

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 growth in vivo by 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.

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Accession: 069942413

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