期刊
CELLULAR SIGNALLING
卷 54, 期 -, 页码 170-178出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2018.12.005
关键词
DHX33; RNA helicase; PI3K/Akt/mTOR; Glioblastoma
类别
资金
- Science and Technology Innovation Committee of Shenzhen Municipality [JCYJ20170307110713487]
- Guangdong Provincial Science and Technology Department [2017A020211024]
Human Glioblastoma is one deadly disease; the median survival time is reported to be 13.9 months after treatment. In the present study, we discovered that DHX33 is highly expressed in 84% of all Glioblastoma multiforme (GBM). Knockdown of DHX33 led to significant reduced proliferation and migration in glioblastoma cells in vitro and in vivo. Mechanistically, DHX33 regulated a set of critical genes involved in cell cycle and cell migration to promote glioblastoma development. Additionally, DHX33 was found to be induced by inhibitors of PI3K and mTOR whose activation has been detected in 50% of glioblastoma. Overexpression of wild type DHX33 protein, but not the helicase dead mutant, confers resistance to mTOR inhibitors in glioblastoma cells. DHX33 probably functions as a critical regulator to promote GBM development. Our results highlight its therapeutic potential in treating GBM.
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