Investigators from the University of Central Florida (Orlando, USA) studied the role of the receptor channel protein TRPC6 (transient receptor potential 6) in the progression of GBM. They reported in the December 22, 2009 online edition of the journal Cancer Research that under conditions of hypoxia TRPC6 was required for the development of an aggressive tumor phenotype. This conclusion was reached due to the finding that knockdown of TRPC6 expression inhibited glioma growth, invasion, and angiogenesis.

Functionally, TRPC6 caused a sustained elevation of intracellular calcium that was coupled to the activation of the NFAT (calcineurin-nuclear factor of activated T-cell) pathway. Pharmacologic inhibition of the calcineurin-NFAT pathway substantially reduced the development of malignant GBM phenotypes under hypoxia. Clinically, expression of TRPC6 was elevated in GBM specimens in comparison with normal tissues.

“Collectively, our studies indicate that TRPC6 is a key mediator of tumor growth of GBM. It may be a promising therapeutic target in the treatment of human GBM,” said Dr. Sic L. Chan, assistant professor of neuroscience at the University of Central Florida.

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