Abstract
Glioblastoma multiforme (GBM) is one of the most malignant cancers in human brain. The prognosis of GBM is extremely poor because it is resistant to radiotherapy and chemotherapy. Improving understanding of the tumor biology brings some new hope to the treatment of GBM. In this review, we discuss the evidence that FoxM1 promotes the development and progression of GBM by regulating key factors involved in cell proliferation, epithelial to mesenchymal transition (EMT), invasion, angiogenesis and upregulating Wnt/β-catenin signalling. Our recent experimental findings are also summarized to prove that FoxM1 is a novel therapeutic target against GBM.
Keywords: Glioblastoma, tumorigenesis, EMT, invasion, angiogenesis, FoxM1, Wnt/β-catenin signaling.
Current Pharmaceutical Design
Title:Glioblastoma Multiforme Formation and EMT: Role of FoxM1 Transcription Factor
Volume: 21 Issue: 10
Author(s): Zhongyong Wang, Sicong Zhang, Timothy L Siu and Suyun Huang
Affiliation:
Keywords: Glioblastoma, tumorigenesis, EMT, invasion, angiogenesis, FoxM1, Wnt/β-catenin signaling.
Abstract: Glioblastoma multiforme (GBM) is one of the most malignant cancers in human brain. The prognosis of GBM is extremely poor because it is resistant to radiotherapy and chemotherapy. Improving understanding of the tumor biology brings some new hope to the treatment of GBM. In this review, we discuss the evidence that FoxM1 promotes the development and progression of GBM by regulating key factors involved in cell proliferation, epithelial to mesenchymal transition (EMT), invasion, angiogenesis and upregulating Wnt/β-catenin signalling. Our recent experimental findings are also summarized to prove that FoxM1 is a novel therapeutic target against GBM.
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Cite this article as:
Wang Zhongyong, Zhang Sicong, Siu L Timothy and Huang Suyun, Glioblastoma Multiforme Formation and EMT: Role of FoxM1 Transcription Factor, Current Pharmaceutical Design 2015; 21 (10) . https://dx.doi.org/10.2174/1381612821666141211115949
DOI https://dx.doi.org/10.2174/1381612821666141211115949 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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