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Antiproliferative and apoptotic effects of telmisartan in human glioma cells
Yung-Lung Chang1, Chung-Hsing Chou2, Yao-Feng Li3
1Department of Biochemistry, National Defense Medical Center, Taipei, 11490, Taiwan.
Abstract:
Glioblastoma is the most common primary central nervous system tumor in adults. Angiotensin II receptor blockers (ARBs) are broadly applied to treat hypertension. Moreover, research has revealed that ARBs have the capacity to suppress the growth of several cancer types. In this study, we assessed the effects of three ARBs with the ability to cross the blood brain barrier (telmisartan, valsartan and fimasartan) on cell proliferation in three glioblastoma multiforme (GBM) cell lines. Telmisartan markedly suppressed the proliferation, migration, and invasion of these three GBM cell lines. Microarray data analysis revealed that telmisartan regulates DNA replication, mismatch repair, and the cell cycle pathway in GBM cells. Furthermore, telmisartan induced G0/G1 phase arrest and apoptosis. The bioinformatic analysis and western blotting results provide evidence that SOX9 is a downstream target of telmisartan. Telmisartan also suppressed tumor growth in vivo in an orthotopic transplant mouse model. Therefore, telmisartan is a potential treatment for human GBM.
Insights
Telmisartan, an angiotensin II receptor blocker (ARB), effectively suppressed glioblastoma multiforme (GBM) growth, proliferation, and invasion. This study suggests telmisartan as a promising therapeutic agent for treating human GBM.
Area of Science:
- Neuro-oncology
- Pharmacology
Background:
- Glioblastoma multiforme (GBM) is a prevalent and aggressive primary brain tumor.
- Angiotensin II receptor blockers (ARBs) are established antihypertensive drugs with emerging anti-cancer properties.
Purpose of the Study:
- To investigate the efficacy of blood-brain barrier-penetrating ARBs (telmisartan, valsartan, fimasartan) against glioblastoma.
- To elucidate the molecular mechanisms underlying telmisartan's anti-GBM effects.
Main Methods:
- Assessment of ARB effects on GBM cell proliferation, migration, and invasion in vitro.
- Microarray analysis to identify regulated pathways.
- In vivo efficacy testing using an orthotopic GBM mouse model.
Main Results:
- Telmisartan significantly inhibited GBM cell proliferation, migration, and invasion.
- Telmisartan modulated DNA replication, mismatch repair, and cell cycle pathways, inducing G0/G1 arrest and apoptosis.
- SOX9 was identified as a downstream target of telmisartan.
- Telmisartan demonstrated in vivo tumor growth suppression.
Conclusions:
- Telmisartan exhibits potent anti-cancer activity against glioblastoma multiforme.
- Telmisartan's therapeutic potential in GBM warrants further clinical investigation.
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