Suppression of TRPM7 Inhibits Proliferation, Migration, and Invasion of Malignant Human Glioma Cells
Summary Background Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor with a dismal prognosis. Despite intensive study on tumor biology, the underlying mechanisms of the unlimited proliferation and progressive local invasion are still poorly understood, and no effect...
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Veröffentlicht in: | CNS neuroscience & therapeutics 2015-03, Vol.21 (3), p.252-261 |
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Sprache: | eng |
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Zusammenfassung: | Summary
Background
Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor with a dismal prognosis. Despite intensive study on tumor biology, the underlying mechanisms of the unlimited proliferation and progressive local invasion are still poorly understood, and no effective treatment has been developed for GBM patients.
Aims
We determine the role of TRPM7 channels in the growth, migration, and infiltration of malignant glioma cells.
Methods
Using a combination of RT‐PCR, Western blot, and patch‐clamp techniques, we demonstrated the expression of functional TRPM7 channels of A172 cells, a human glioma cell line, as well as in human glioma tissues. Furthermore, we evaluated the role of TRPM7 in growth, migration, and infiltration of A172 cells with MTT and transwell migration and invasion assays.
Results
We showed the expression of functional TRPM7 channels in both A172 cells and human glioma tissues. Suppression of TRPM7 expression with TRPM7‐siRNA dramatically reduced the proliferation, migration, and invasion of A172 cells. Pharmacological inhibition of TRPM7 channel with 2‐aminoethoxydiphenyl borate (2‐APB) showed a similar effect as TRPM7‐siRNA.
Conclusion
We demonstrate that human glioma cells express functional TRPM7 channel and that activation of this channel plays an important role in the proliferation, migration, and invasion of malignant glioma cells. TRPM7 channel may represent a novel and promising target for therapeutic intervention of malignant glioma. |
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ISSN: | 1755-5930 1755-5949 |
DOI: | 10.1111/cns.12354 |