Peng Ge1, Lei Cao2, Ming Zheng3, Yuejuan Yao3, Wei Wang3, Xin Chen4. 1. Shaanxi Provincial Research Center for the Project of Prevention and Treatment of Respiratory Diseases, Xi'an Medical University, Xi'an City, Shaanxi Province, China; Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Xi'an Medical University, Xi'an City, Shaanxi Province, China. 2. Department of Gynecology, The Second Affiliated Hospital of Xi'an Medical University, Xi'an City, Shaanxi Province, China. 3. Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Xi'an Medical University, Xi'an City, Shaanxi Province, China. 4. Shaanxi Provincial Research Center for the Project of Prevention and Treatment of Respiratory Diseases, Xi'an Medical University, Xi'an City, Shaanxi Province, China; Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Xi'an Medical University, Xi'an City, Shaanxi Province, China. Electronic address: g18792929399@163.com.
Abstract
BACKGROUND: Long non-coding RNAs (lncRNAs) are involved in the occurrence and progression of multiple cancers, including non-small cell lung cancer (NSCLC). Herein, we explored the exact role and underlying mechanism of lncRNA small nucleolar RNA host gene 1 (SNHG1) in NSCLC. METHODS: The levels of SNHG1, microRNA-330-5p (miR-330-5p) and doublecortin-like kinase 1 (DCLK1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was carried out to measure the chemoresistance and proliferation of NSCLC cells. The metastasis and apoptosis of NSCLC cells were examined by transwell migration and invasion assays and flow cytometry. Western blot assay was conducted to detect the levels of proliferation-associated proteins and DCLK1. The interaction between miR-330-5p and SNHG1 or DCLK1 was predicted by StarBase and microT_CDS databases. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to validate these interactions. In vivo chemosensitivity experiment was conducted to assess the function of SNHG1 in the chemoresistance of NSCLC in vivo. RESULTS: SNHG1 was dramatically up-regulated in cisplatin (DDP)-resistant NSCLC tissues and cells. SNHG1 promoted the DDP resistance and malignant behaviors of NSCLC cells. SNHG1 functioned through targeting miR-330-5p, and si-SNHG1-mediated effects in NSCLC cells were attenuated by the addition of in-miR-330-5p. DCLK1 messenger RNA (mRNA) could directly bind to miR-330-5p, and miR-330-5p acted as a tumor suppressor in NSCLC through down-regulating DCLK1. SNHG1 silencing elevated the DDP sensitivity of NSCLC cells in vivo. CONCLUSION: SNHG1 elevated DDP resistance and malignant potential of NSCLC cells through elevating the level of DCLK1 via sponging miR-330-5p.
BACKGROUND: Long non-coding RNAs (lncRNAs) are involved in the occurrence and progression of multiple cancers, including non-small cell lung cancer (NSCLC). Herein, we explored the exact role and underlying mechanism of lncRNA small nucleolar RNA host gene 1 (SNHG1) in NSCLC. METHODS: The levels of SNHG1, microRNA-330-5p (miR-330-5p) and doublecortin-like kinase 1 (DCLK1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was carried out to measure the chemoresistance and proliferation of NSCLC cells. The metastasis and apoptosis of NSCLC cells were examined by transwell migration and invasion assays and flow cytometry. Western blot assay was conducted to detect the levels of proliferation-associated proteins and DCLK1. The interaction between miR-330-5p and SNHG1 or DCLK1 was predicted by StarBase and microT_CDS databases. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to validate these interactions. In vivo chemosensitivity experiment was conducted to assess the function of SNHG1 in the chemoresistance of NSCLC in vivo. RESULTS:SNHG1 was dramatically up-regulated in cisplatin (DDP)-resistant NSCLC tissues and cells. SNHG1 promoted the DDP resistance and malignant behaviors of NSCLC cells. SNHG1 functioned through targeting miR-330-5p, and si-SNHG1-mediated effects in NSCLC cells were attenuated by the addition of in-miR-330-5p. DCLK1 messenger RNA (mRNA) could directly bind to miR-330-5p, and miR-330-5p acted as a tumor suppressor in NSCLC through down-regulating DCLK1. SNHG1 silencing elevated the DDP sensitivity of NSCLC cells in vivo. CONCLUSION:SNHG1 elevated DDP resistance and malignant potential of NSCLC cells through elevating the level of DCLK1 via sponging miR-330-5p.
Authors: Dan Li; Xiaoli Liu; Ni Jiang; Di Ke; Qiang Guo; Kui Zhai; Hao Han; Xue Xiao; Tengyang Fan Journal: Am J Cancer Res Date: 2022-07-15 Impact factor: 5.942