Shu-Li Liu1, Mao-Hua Chen2, Xiao-Bo Wang1, Rong-Kai You1, Xue-Wei An3, Qiu Zhao4, Ren-Shu Wang1. 1. Department of Intensive Care Unit, Wenzhou Central Hospital, Wenzhou Medical University, Wenzhou 325000, China. 2. Neurosurger Department, Wenzhou Central Hospital, Wenzhou Medical University, Wenzhou 325000, China. 3. Wenzhou Seventh People's Hospital, Wenzhou 325000, China. 4. Emergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Abstract
BACKGROUND: Glioma, one of the most prevalent and aggressive cancers, is regulated by long noncoding RNAs (lncRNAs). This study aims to research the functional mechanism of lncRNA PCGEM1 involved in glioma progression. METHODS: Expression levels of PCGEM1, miR-539-5p and CDK6 were analyzed by qRT-PCR in NHA, U251, U87, and LN229 cells or glioma tissues. shRNAs were used to knock down PCGEM1 in U251 and LN229 cells. Kaplan-Meier curve and log rank test were utilized to examine survival rate. CCK8 (Cell Counting Kit-8) assay, colony formation assay and EdU staining were conducted to detect cell proliferation. Transwell assay was performed to evaluate cell migration and invasion. Luciferase reporter assay was conducted to assess RNA interaction between PCGEM1 and miR-539-5p. Nude mice were used for tumor xenograft assay. RESULTS: LncRNA PCGEM1 was upregulated in glioma tissues and tumor cell lines. PCGEM1 upregulation predicted unsatisfactory prognosis. PCGEM1 knockdown inhibited proliferation, colony formation, migration and invasion. PCGEM1 knockdown delayed tumor growth in vivo. PCGEM1 played as a competing endogenous RNA (ceRNA) for miR-539-5p to promote CDK6 expression. MiR-539-5p mimics repressed glioma progression while CDK6 overexpression reversed the roles of PCGEM1 knockdown. CONCLUSION: PCGEM1 knockdown suppressed glioma progression through sponging miR-539-5p and regulating CDK6 expression, implying PCGEM1 as a potential therapeutic target.
BACKGROUND:Glioma, one of the most prevalent and aggressive cancers, is regulated by long noncoding RNAs (lncRNAs). This study aims to research the functional mechanism of lncRNA PCGEM1 involved in glioma progression. METHODS: Expression levels of PCGEM1, miR-539-5p and CDK6 were analyzed by qRT-PCR in NHA, U251, U87, and LN229 cells or glioma tissues. shRNAs were used to knock down PCGEM1 in U251 and LN229 cells. Kaplan-Meier curve and log rank test were utilized to examine survival rate. CCK8 (Cell Counting Kit-8) assay, colony formation assay and EdU staining were conducted to detect cell proliferation. Transwell assay was performed to evaluate cell migration and invasion. Luciferase reporter assay was conducted to assess RNA interaction between PCGEM1 and miR-539-5p. Nude mice were used for tumor xenograft assay. RESULTS: LncRNA PCGEM1 was upregulated in glioma tissues and tumor cell lines. PCGEM1 upregulation predicted unsatisfactory prognosis. PCGEM1 knockdown inhibited proliferation, colony formation, migration and invasion. PCGEM1 knockdown delayed tumor growth in vivo. PCGEM1 played as a competing endogenous RNA (ceRNA) for miR-539-5p to promote CDK6 expression. MiR-539-5p mimics repressed glioma progression while CDK6 overexpression reversed the roles of PCGEM1 knockdown. CONCLUSION:PCGEM1 knockdown suppressed glioma progression through sponging miR-539-5p and regulating CDK6 expression, implying PCGEM1 as a potential therapeutic target.
Authors: J Zhang; H Y Jin; Y Wu; Z C Zheng; S Guo; Y Wang; D Yang; X Y Meng; X Xu; Y Zhao Journal: Clin Transl Oncol Date: 2019-01-28 Impact factor: 3.405
Authors: Wing Pui Tsang; Enders K O Ng; Simon S M Ng; Hongchuan Jin; Jun Yu; Joseph J Y Sung; Tim Tak Kwok Journal: Carcinogenesis Date: 2009-11-19 Impact factor: 4.944