title: MicroRNA-610 suppresses the proliferation of human glioblastoma cells by repressing CCND2 and AKT3.
abstract: Previous studies have shown that microRNA (miR)-610 is crucial in a variety of biological processes in various types of human cancer cells. However, the role of this microRNA in glioblastoma (GBM) is presently unclear. In this study, the role of miR‑610 in cell proliferation was investigated in GBM. It was demonstrated that miR‑610 expression is markedly downregulated in GBM cells and GBM tissues compared with normal human astrocytes (NHAs) and normal brain tissue, respectively. Ectopic expression of miR‑610 reduced the proliferation and anchorage‑independent growth of GBM cells, whereas inhibition of miR‑610 promoted this effect. Bioinformatics analysis further revealed cyclin D2 (CCND2) and AKT3, putative tumor promoters, as potential targets of miR‑610. Data from reporter assays showed that miR‑610 directly binds to the 3'‑untranslated region of CCND2 and AKT3 mRNA, and represses their expression at the transcriptional and translational levels. In conclusion, the data provide compelling evidence that miR‑610 functions as an anti‑onco‑miRNA, which is important in inhibiting cell proliferation in GBM, and its anti‑oncogenic effects are mediated chiefly through direct suppression of CCND2 and AKT3 expression.
authors.affiliation: Department of Pharmacy, Qingdao Women and Children Hospital, Qingdao, Shandong 266034, P.R. China.
authors.forename: Xiaomei
authors.initials: X
authors.lastname: Mo
authors.affiliation: Heart Center, Qingdao Women and Children Hospital, Qingdao, Shandong 266034, P.R. China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Cao
authors.affiliation: Department of Hematology, Qingdao Women and Children Hospital, Qingdao, Shandong 266034, P.R. China.
authors.forename: Hui
authors.initials: H
authors.lastname: Liang
authors.affiliation: Department of Neurosurgery, The First Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
authors.forename: Jianmin
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Laboratory Medicine of Qingdao Municipal Hospital, Qingdao, Shandong 266011, P.R. China.
authors.forename: Huahui
authors.initials: H
authors.lastname: Li
authors.affiliation: Department of Laboratory Medicine of Qingdao Municipal Hospital, Qingdao, Shandong 266011, P.R. China.
authors.forename: Fenghai
authors.initials: F
authors.lastname: Liu
mesh_terms: D020413:3' Untranslated Regions / Q000235:genetics; D000328:Adult; D000368:Aged; D001483:Base Sequence; D002453:Cell Cycle / Q000235:genetics; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D056742:Cyclin D2 / Q000378:metabolism*; D015536:Down-Regulation / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic; D005909:Glioblastoma / Q000235:genetics* / Q000473:pathology*; D006801:Humans; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D008875:Middle Aged; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D014162:Transfection
chemical_list: D020413:3' Untranslated Regions; C080336:CCND2 protein, human; D056742:Cyclin D2; C575383:MIRN610 microRNA, human; D035683:MicroRNAs; C491754:AKT3 protein, human; D051057:Proto-Oncogene Proteins c-akt