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MiR-29c inhibits glioma cell proliferation, migration, invasion and angiogenesis.
Fan, Yue-chao; Mei, Peng-jin; Chen, Chen; Miao, Fa-an; Zhang, Hui; Li, Zhong-lin.
Afiliación
  • Fan YC; Department of Neurosurgery, The Affiliated Hospital of Xuzhou Medical College, 99 West Huai-hai Road, Xuzhou, 221002, Jiangsu, China, fanyuechaoxyfy@163.com.
J Neurooncol ; 115(2): 179-88, 2013 Nov.
Article en En | MEDLINE | ID: mdl-23943502
ABSTRACT
Previous studies reported that miR-29c is significantly downregulated in several tumors. However, little is known about the effect and molecular mechanisms of action of miR-29c in human glioma. Using quantitative RT-PCR, we demonstrated that miR-29c was significantly downregulated in glioma cell lines and human primary glioma tissues, compared to normal human astrocytes and matched non-tumor associated tissues (P < 0.05, χ(2) test). Overexpression of miR-29c dramatically reduced the proliferation and caused cessation of cell cycle. The reduced cell proliferation is due to G1 phase arrest as cyclin D1 and cyclin E are diminished whereas p27 and p21 are upregulated. We further demonstrated that miR-29c overexpression suppressed the glioma cell migration and invasion abilities by targeting MMP-2. In addition, we also found that overexpression of miR-29c sharply inhibited angiogenesis, which correlated with down-regulation of VEGF. The data indicate that miR-29c may be a tumor suppressor involved in the progression of glioma.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Encefálicas / Movimiento Celular / MicroARNs / Proliferación Celular / Glioma / Neovascularización Patológica Límite: Humans Idioma: En Revista: J Neurooncol Año: 2013 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Encefálicas / Movimiento Celular / MicroARNs / Proliferación Celular / Glioma / Neovascularización Patológica Límite: Humans Idioma: En Revista: J Neurooncol Año: 2013 Tipo del documento: Article
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