title: Downregulation of GRIM-19 promotes growth and migration of human glioma cells.
abstract: It has become increasingly clear that there are notable parallels between normal development and tumorigenesis. Glioma is a classic model that links between tumorigenesis and development. We evaluated the expression of GRIM-19, a novel gene essential for normal development, in various grades of gliomas and several human glioma cell lines. We showed that GRIM-19 mRNA and protein expression were markedly lower in gliomas than in control brain tissues and negatively correlated with the malignancy of gliomas. Downregulation of GRIM-19 in glioma cells significantly enhanced cell proliferation and migration, whereas overexpression of GRIM-19 showed the opposite effects. We also showed that the activation of signal transducer and activator of transcription 3 (STAT3) and the expression of many STAT3-dependent genes were regulated by the expression of GRIM-19. In addition, GRIM-19 exerted its role probably through the non-STAT3 signaling pathway. Collectively, our data suggest that most gliomas expressed GRIM-19 at low levels, which may play a major role in tumorigenesis in the brain.
authors.affiliation: Key Laboratory of Ministry of Education for Experimental Teratology, Department of Histology and Embryology, Shandong University School of Medicine, Jinan, China.
authors.forename: Yanmin
authors.initials: Y
authors.lastname: Zhang
authors.forename: Hongbo
authors.initials: H
authors.lastname: Hao
authors.forename: Shidou
authors.initials: S
authors.lastname: Zhao
authors.forename: Qian
authors.initials: Q
authors.lastname: Liu
authors.forename: Qiuhuan
authors.initials: Q
authors.lastname: Yuan
authors.forename: Shilei
authors.initials: S
authors.lastname: Ni
authors.forename: Fuwu
authors.initials: F
authors.lastname: Wang
authors.forename: Shangming
authors.initials: S
authors.lastname: Liu
authors.forename: Liyan
authors.initials: L
authors.lastname: Wang
authors.forename: Aijun
authors.initials: A
authors.lastname: Hao
mesh_terms: D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D001921:Brain / Q000378:metabolism; D001932:Brain Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D002455:Cell Division / Q000502:physiology; D002465:Cell Movement / Q000502:physiology; D051546:Cyclooxygenase 2; D015972:Gene Expression Regulation, Neoplastic; D005909:Glioblastoma / Q000378:metabolism / Q000473:pathology; D005910:Glioma / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D009247:NADH, NADPH Oxidoreductases / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D009419:Nerve Tissue Proteins / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D010766:Phosphorylation; D011499:Protein Processing, Post-Translational; D034622:RNA Interference; D011993:Recombinant Fusion Proteins / Q000502:physiology; D050796:STAT3 Transcription Factor / Q000502:physiology; D051742:Transcription Factor CHOP; D014407:Tumor Cells, Cultured / Q000473:pathology; D014410:Tumor Stem Cell Assay
chemical_list: D051017:Apoptosis Regulatory Proteins; C497249:DDIT3 protein, human; D009363:Neoplasm Proteins; D009419:Nerve Tissue Proteins; D011993:Recombinant Fusion Proteins; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D051742:Transcription Factor CHOP; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D009247:NADH, NADPH Oxidoreductases; C439057:NDUFA13 protein, human