title: MiR-454 inhibited cell proliferation of human glioblastoma cells by suppressing PDK1 expression.
abstract: It has been well documented that aberrant expression of microRNAs is associated with carcinogenesis of glioblastoma (GBM), however the underlying mechanisms are not clear. In this present study, we aimed to clarify the biological function of miR-454 in GBM. MiR-454 was identified to be significantly down-regulated in GBM primary tumors and cell lines. Overexpression of miR-454 in GBM cells resulted in arresting cells at G0/G1 phase and thus inhibiting cell proliferation. Bioinformatic analysis predicted 3-phosphoinositide-dependent protein kinase-1 (PDK1) as a target of miR-454 which acted as a tumor promoter gene. Increased miR-454 significantly repressed PDK1 expression, and then regulating cell proliferation and cell cycle regulators, down-regulation of Cyclin D1 and p-pRb and p21 was up-regulated. Taken together, our study has revealed miR-454 as a tumor suppressor in GBM.
authors: Department of Neurosurgery, Qilu Hospital of Shandong University, Jinan, 250012 Shandong, PR China; Department of Neurosurgery, Liaocheng People's Hospital, Liaocheng 252000, Shandong, PR China.
authors: Baojun
authors: B
authors: Fang
authors: Department of Neurosurgery, Qilu Hospital of Shandong University, Jinan, 250012 Shandong, PR China; Department of Neurosurgery, Liaocheng People's Hospital, Liaocheng 252000, Shandong, PR China.
authors: Jianxin
authors: J
authors: Zhu
authors: Department of Neurosurgery, Liaocheng People's Hospital, Liaocheng 252000, Shandong, PR China.
authors: Yunhua
authors: Y
authors: Wang
authors: Department of Neurosurgery, Liaocheng People's Hospital, Liaocheng 252000, Shandong, PR China.
authors: Fengyang
authors: F
authors: Geng
authors: Department of Neurosurgery, Qilu Hospital of Shandong University, Jinan, 250012 Shandong, PR China. Electronic address: gangliqilu@163.com.
authors: Gang
authors: G
authors: Li
mesh_terms: D020413:3' Untranslated Regions; D064413:3-Phosphoinositide-Dependent Protein Kinases / Q000235:genetics* / Q000378:metabolism; D001665:Binding Sites; D001932:Brain Neoplasms / Q000201:enzymology / Q000235:genetics* / Q000473:pathology; D059447:Cell Cycle Checkpoints; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D019295:Computational Biology; D019938:Cyclin D1 / Q000235:genetics / Q000378:metabolism; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000235:genetics / Q000378:metabolism; D015971:Gene Expression Regulation, Enzymologic; D015972:Gene Expression Regulation, Neoplastic; D005910:Glioma / Q000201:enzymology / Q000235:genetics* / Q000473:pathology; D006801:Humans; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D010766:Phosphorylation; D016160:Retinoblastoma Protein / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D013997:Time Factors; D014162:Transfection
chemical_list: D020413:3' Untranslated Regions; C530104:CCND1 protein, human; C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; C583712:MIRN454 microRNA, human; D035683:MicroRNAs; D016160:Retinoblastoma Protein; D019938:Cyclin D1; D064413:3-Phosphoinositide-Dependent Protein Kinases; C578562:PDPK1 protein, human
keywords: Cell cycle; Cell proliferation; Glioblastoma; MiR-454; PDK1