Overexpression of RKIP Inhibits Cell Invasion in Glioma Cell Lines through Upregulation of miR-98
| Autor: | Renjun Peng, Quan Cheng, Zhiming Ma, Haipeng Xi, Bing Jiang, Zigui Chen |
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| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
Article Subject
lcsh:Medicine Phosphatidylethanolamine Binding Protein Tumor initiation Biology General Biochemistry Genetics and Molecular Biology HMGA2 Glioma Cell Line Tumor microRNA medicine Humans Metastasis suppressor Neoplasm Invasiveness Cell Proliferation General Immunology and Microbiology Cell growth HMGA2 Protein lcsh:R General Medicine medicine.disease Cell biology Gene Expression Regulation Neoplastic MicroRNAs Cancer cell Cancer research biology.protein Signal transduction Signal Transduction Research Article |
| Zdroj: | BioMed Research International, Vol 2013 (2013) BioMed Research International |
| ISSN: | 2314-6141 2314-6133 |
| Popis: | Raf-1 kinase inhibitor protein (RKIP) is a tumor and metastasis suppressor in cancer cells. MicroRNAs (miRNAs) have been suggested to play a vital role in tumor initiation and progression by negatively regulating oncogenes and tumor suppressors. Quite recently, studies have identified some miRNAs operating to promote or suppress tumor invasion or metastasis via regulating metastasis-related genes, providing potential therapeutic targets on antimetastasis strategy. In this study, we found that the expression of RKIP and miR-98 in glioma tissues were significantly lower than that in normal brain tissues. Overexpression of RKIP upregulated miR-98 expression and inhibited glioma cell invasion and miR-98 target gene HMGA2 but had no effect in glioma cell proliferation. Moreover, forced expression of miR-98 accelerated the inhibition of glioma cell invasion and the expression of HMGA2 also had no effect in glioma cell proliferation. Our findings newly described RKIP/miR-98 to HMGA2 link and provided a potential mechanism for glioma cell invasion. RKIP and miR-98 may illustrate the potential therapeutic utility of signaling pathway signatures. |
| Databáze: | OpenAIRE |
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