Journal
MARINE DRUGS
Volume 17, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/md17100587
Keywords
venom peptide; liver cancer; terebrid snail; TRP channel; Cox-2
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Funding
- Camille and Henry Dreyfus Teacher-Scholar Award
- NSF [CHE-1247550]
- CTSC Pilot Award from Weill Cornell Medicine [NIH-1UL1TR002384-01]
- NIH-NIMHD [MD007599]
- NIH/NIMHD [8 G 12 MD007599]
- NIH/NCI [U54CA221704]
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Increasingly cancer is being viewed as a channelopathy because the passage of ions via ion channels and transporters mediate the regulation of tumor cell survival, death, and motility. As a result, a potential targeted therapy for cancer is to use venom peptides that are selective for ion channels and transporters overexpressed in tumor cells. Here we describe the selectivity and mechanism of action of terebrid snail venom peptide, Tv1, for treating the most common type of liver cancer, hepatocellular carcinoma (HCC). Tv1 inhibited the proliferation of murine HCC cells and significantly reduced tumor size in Tv1-treated syngeneic tumor-bearing mice. Tv1's mechanism of action involves binding to overexpressed transient receptor potential (TRP) channels leading to calcium dependent apoptosis resulting from down-regulation of cyclooxygenase-2 (COX-2). Our findings demonstrate the importance of modulating ion channels and the unique potential of venom peptides as tumor specific ligands in the quest for targeted cancer therapies.
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