Static magnetic field inhibits epithelial mesenchymal transition and metastasis of glioma

Abstract Gliomas exhibit suboptimal responses to conventional treatments, with tumor cell migration remaining a significant challenge in therapy. Epithelial-mesenchymal transition (EMT) is crucial for glioma cell invasion, and transforming growth factor β1(TGF-β1) is a key factor promoting prolifera...

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Main Authors: Ziyu Sun, Wenxuan Zhao, Xifeng Fei, Bao He, Lei Shi, Zhen Zhang, Shizhong Cai
Format: Article
Language:English
Published: Nature Portfolio 2025-04-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-96047-x
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Summary:Abstract Gliomas exhibit suboptimal responses to conventional treatments, with tumor cell migration remaining a significant challenge in therapy. Epithelial-mesenchymal transition (EMT) is crucial for glioma cell invasion, and transforming growth factor β1(TGF-β1) is a key factor promoting proliferation, migration, and EMT in glioblastoma (GBM). Although magnetic fields are widely used in the diagnosis and treatment of various diseases, their effects on EMT in glioma cells remain unclear. In this study, we investigated whether a static magnetic field (SMF) could inhibit EMT and metastasis in glioma cells. Cellular functional assays using the U251 and U87 glioma cell lines were performed to investigate their functional and phenotypic changes. Results showed that TGF-β1 treatment increased the invasion and migration capabilities of glioma cells, while simultaneously reducing apoptosis. However, when SMF was combined with TGF-β1 treatment, a significant reduction in cell migration and invasion was observed, along with an increase in apoptosis. Additionally, this combination treatment significantly decreased the protein expression of mesenchymal markers N-cadherin and β-catenin, as well as reduced the levels of the matrix metalloproteinase (MMP)-2. Collectively, these findings suggest that SMFs may attenuate glioma cell metastasis by inhibiting EMT. Therefore, SMFs could represent a promising therapeutic strategy for diminishing glioma metastasis.
ISSN:2045-2322