MSX1 inhibits cell migration and invasion through regulating the Wnt/β-catenin pathway in glioblastoma
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Updated: Apr 5, 2026

Co-culture of Glioblastoma Stem-like Cells on Patterned Neurons to Study Migration and Cellular Interactions
Published on: February 24, 2021
Haiquan Tao1,2, Li Guo3, Lifeng Chen1
1Department of Neurosurgery, The People's Liberation Army General Hospital, 28 Fuxin Road, Haidian District, Beijing, 100000, China.
Abstract:
Glioblastoma is a type of primary brain tumor with poor prognosis. The hallmark phenotype of glioblastoma is its aggressive invasion. Understanding the molecular mechanism of the invasion behavior of glioblastoma is essential for the development of effective treatment of the disease. In our present study, we found that the expression levels of a homeobox transcription factor, MSX1, were significantly reduced in glioblastoma compared to normal brain tissues. The levels of MSX1 in glioblastoma tissues were also correlated with the survival of the patients. In cultured glioblastoma cells, MSX1 was a negative regulator of cell migration and invasion. Loss of MSX1 enhanced cell migration and induced mesenchymal transition as characterized by the downregulation of E-cadherin and the upregulation of N-cadherin. Overexpression of MSX1 on the other hand led to the inhibition of both cell migration and mesenchymal transition. We also found that MSX1 was able to inhibit the Wnt/β-catenin signaling pathway, and that the ability to regulate the Wnt/β-catenin signaling pathway is critical for MSX1 to suppress glioblastoma cell migration and invasion.
Insights
MSX1, a key transcription factor, is reduced in glioblastoma, hindering its ability to suppress tumor cell invasion. Restoring MSX1 may offer a new therapeutic strategy for this aggressive brain cancer.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Cancer Genetics
Background:
- Glioblastoma is an aggressive primary brain tumor with a poor prognosis.
- Tumor cell invasion is a critical factor in glioblastoma progression and treatment resistance.
- Understanding the molecular drivers of glioblastoma invasion is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the role of the homeobox transcription factor MSX1 in glioblastoma.
- To determine the relationship between MSX1 expression levels and patient survival.
- To elucidate the molecular mechanisms by which MSX1 regulates glioblastoma cell invasion.
Main Methods:
- Quantitative analysis of MSX1 expression in glioblastoma tissues versus normal brain tissues.
- Correlation analysis between MSX1 levels and patient survival data.
- In vitro studies using cultured glioblastoma cells to assess the effects of MSX1 modulation on cell migration, invasion, and epithelial-mesenchymal transition (EMT).
- Investigation of MSX1's impact on the Wnt/β-catenin signaling pathway.
Main Results:
- MSX1 expression is significantly reduced in glioblastoma tissues compared to normal brain.
- Lower MSX1 levels correlate with reduced patient survival.
- MSX1 acts as a negative regulator of glioblastoma cell migration and invasion.
- Loss of MSX1 promotes EMT, evidenced by altered E-cadherin and N-cadherin expression.
- MSX1 overexpression inhibits cell migration, invasion, and EMT.
- MSX1 suppresses glioblastoma cell invasion by inhibiting the Wnt/β-catenin signaling pathway.
Conclusions:
- MSX1 plays a critical role in suppressing glioblastoma cell invasion and metastasis.
- Reduced MSX1 expression is linked to poor prognosis in glioblastoma patients.
- Targeting MSX1 or its downstream pathways may represent a novel therapeutic strategy for glioblastoma.
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