Immune responsive gene 1, a novel oncogene, increases the growth and tumorigenicity of glioma
| Autor: | Shizhong Zhang, Jun Pan, Tianzhu Liu, Xiaoyong Zhao, Hongchao Xu, Zhilin Yin, Chunnan Lin |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Adult
Male Cancer Research Carboxy-Lyases Mice Nude Cell Cycle Proteins Biology medicine.disease_cause Mice Cyclin D1 RNA interference Cell Line Tumor Glioma medicine Animals Humans RNA Small Interfering Aged Aged 80 and over Gene knockdown Oncogene Proteins Oncogenes General Medicine Middle Aged Cell cycle medicine.disease Oncology Cancer research biology.protein Female Cyclin-dependent kinase 6 Carcinogenesis Neoplasm Transplantation Signal Transduction |
| Zdroj: | Oncology Reports. 32:1957-1966 |
| ISSN: | 1791-2431 1021-335X |
| DOI: | 10.3892/or.2014.3474 |
| Popis: | Immune responsive gene 1 (IRG1) is highly expressed in mammalian macrophages during inflammation. However, the role of IRG1 in tumorigenesis remains unclear. In the present study, we aimed to clarify the epigenetic regulation and biological functions of IRG1 in glioma. We found that the expression level of IRG1 influenced the WHO stage in 140 glioma patients. Overexpression of IRG1 increased the growth, invasion, and tumorigenesis in U251 and SHG-44 glioma cells both in vitro and in vivo. Suppression of IRG1 expression by si-IRG1 decreased the levels of cell cycle regulatory proteins, namely, E2F1, p21, CDK4, CDK6 and cyclin D1. Knockdown of IRG1 expression by RNA interference increased E-cadherin expression and decreased the amounts of snail and vimentin. Furthermore, the suppression of IRG1 expression inhibited the expression of NF-κB and STAT3, suggesting a role of IRG1 in regulating the genes associated with these factors and thereby contributing to a decrease in glioma cell proliferation, migration and invasion. Collectively, our findings revealed that IRG1 is a candidate oncogene that is amplified in glioma and is involved in novel mechanisms that influence glioma pathogenesis. |
| Databáze: | OpenAIRE |
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