title: MicroRNA-16 suppresses epithelial-mesenchymal transition‑related gene expression in human glioma.
abstract: Glioma is one of the most prevalent types of brain tumor and is associated with the highest mortality rate of all CNS cancers. Epithelial‑mesenchymal transition (EMT) has been recognized as an important factor in tumor metastasis. Previously, it has been demonstrated that microRNA-16 (miR-16) has an important role in tumor metastasis in human cancer cell lines. However, the role of miR-16 in epithelial‑mesenchymal transition of human glioma cells remains unclear. In the present study, U87 and U251 glioma cell lines overexpressing miR-16 were established and it was identified that miR-16 suppressed invasion, adhesion, cell cycle, production of interleukin (IL)-6, IL-8 and transforming growth factor-β, and EMT-related gene expression, including vimentin, β-catenin and E-cadherin in miR-16 overexpressing U87 and U251 glioma cells. Furthermore, miR-16 suppressed EMT mainly through the downregulation of p-FAK and p-Akt expression, and nuclear factor-κB and Slug transcriptional activity. Therefore, miR-16 may be an important therapeutic target and predictor for glioma therapy.
authors.affiliation: Department of Clinical Laboratory, Tianjin Huanhu Hospital, Tianjin 300060, P.R. China.
authors.forename: Qin
authors.initials: Q
authors.lastname: Wang
authors.affiliation: Department of Clinical Laboratory, Tianjin Huanhu Hospital, Tianjin 300060, P.R. China.
authors.forename: Xu
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Clinical Laboratory, Tianjin Huanhu Hospital, Tianjin 300060, P.R. China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhu
authors.affiliation: Department of Clinical Laboratory, Tianjin Huanhu Hospital, Tianjin 300060, P.R. China.
authors.forename: Ping
authors.initials: P
authors.lastname: Yang
mesh_terms: D015820:Cadherins / Q000235:genetics; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation / Q000235:genetics; D015536:Down-Regulation / Q000235:genetics; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics*; D051417:Focal Adhesion Kinase 1 / Q000235:genetics; D015870:Gene Expression / Q000235:genetics*; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics*; D005910:Glioma / Q000235:genetics*; D006801:Humans; D015850:Interleukin-6 / Q000235:genetics; D016209:Interleukin-8 / Q000235:genetics; D035683:MicroRNAs / Q000235:genetics*; D016328:NF-kappa B / Q000235:genetics; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics; D000071250:Snail Family Transcription Factors; D014157:Transcription Factors / Q000235:genetics; D016212:Transforming Growth Factor beta / Q000235:genetics; D014746:Vimentin / Q000235:genetics; D051176:beta Catenin / Q000235:genetics
chemical_list: D015820:Cadherins; D015850:Interleukin-6; D016209:Interleukin-8; C505362:MIRN16 microRNA, human; D035683:MicroRNAs; D016328:NF-kappa B; C000604407:SNAI1 protein, human; D000071250:Snail Family Transcription Factors; D014157:Transcription Factors; D016212:Transforming Growth Factor beta; D014746:Vimentin; D051176:beta Catenin; D051417:Focal Adhesion Kinase 1; C496050:PTK2 protein, human; D051057:Proto-Oncogene Proteins c-akt