Activation of Channel Proteins Slows Cancer Cell Growth and Impairs Metastatic Capability

A team of German researchers working with an aggressive breast cancer cell line showed that activation of TRPV1, a transient receptor potential channels protein, caused significant inhibition of cancer cell growth and induced apoptosis and necrosis.

Transient receptor potential (TRP) channels contribute to the regulation of intracellular calcium, which can promote cancer growth in cases of dysregulation of gene transcription and calcium-dependent pro-proliferative or anti-apoptotic mechanisms. Several studies have begun to elucidate the roles of TRPV1, TRPV6, TRPM8, and TRPC1 in cancer progression; however, no study has examined the expression profiles of human TRP channels in breast cancer on a large scale.

In the current study, investigators at Ruhr-Universität Bochum (Germany) worked with the SUM149PT cell culture model system for aggressive triple-negative breast cancer. The investigators activated the cells' TRPV1 receptors by exposing the cell cultures for several hours or days to the compound capsaicin - an active ingredient of pungent substances such as chili peppers - or to helional - a chemical compound used as a perfume in soap and laundry detergent.

Results published in the December 13, 2016, issue of the journal Breast Cancer - Targets and Therapy revealed that activation of the TRPV1 receptor in the cell cultures by capsaicin or helional caused the cancer cells to divide more slowly and to die in increasingly larger numbers. The surviving cells showed decreased motility, which implied that their ability to form metastases was impaired.

"If we could switch on the TRPV1 receptor with specific drugs, this might constitute a new treatment approach for this type of cancer," said senior author Dr. Hanns Hat, professor of cell physiology at Ruhr-Universität Bochum. "An intake via food or inhalation is insufficient for this purpose."

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