Zheng Dong1, Honglai Liu2, Guangli Zhao3. 1. Department of Respiratory Medicine, Linyi Central Hospital, Linyi, China. 2. Department of Thoracic Surgery, Yishui County People's Hospital, Linyi, China. 3. Department of Oncology, Lanling People's Hospital, Linyi, China.
Abstract
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.
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.
Authors: Hong Lee; Sang Hoon Jeong; Hyejin Lee; Cherry Kim; Yoon Jeong Nam; Ja Young Kang; Myeong Ok Song; Jin Young Choi; Jaeyoung Kim; Eun-Kee Park; Yong-Wook Baek; Ju-Han Lee Journal: BMC Pharmacol Toxicol Date: 2022-03-30 Impact factor: 2.483