Journal
MARINE DRUGS
Volume 19, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/md19020093
Keywords
TP4; marine antimicrobial peptide; human synovial sarcoma; calcium overload; mitochondria
Categories
Funding
- Ministry of Science and Technology (MOST
- Taiwan) [MOST109-2320-B-038-010-MY2]
- iEGG
- Animal Biotechnology Center from the Feature Areas Research Center Program within Ministry of Education in Taiwan [MOE-109-S-0023-A]
- Ministry of Science and Technology (Taiwan) [109-2313-B-001-007-MY3, 109-2622-B-001-002-CC1, 108-2313-B-001-006]
- Marine Research Station, Institute of Cellular and Organismic Biology
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Synovial sarcoma is a rare but aggressive soft-tissue sarcoma with limited treatment options. In this study, the marine antimicrobial peptide TP4 showed strong anticancer activity in human synovial sarcoma cells by disrupting oxidative status, promoting mitochondrial hyperpolarization, and causing calcium overload.
Synovial sarcoma is a rare but aggressive soft-tissue sarcoma associated with translocation t(X;18). Metastasis occurs in approximately 50% of all patients, and curative outcomes are difficult to achieve in this group. Since the efficacies of current therapeutic approaches for metastatic synovial sarcoma remain limited, new therapeutic agents are urgently needed. Tilapia piscidin 4 (TP4), a marine antimicrobial peptide, is known to exhibit multiple biological functions, including anti-bacterial, wound-healing, immunomodulatory, and anticancer activities. In the present study, we assessed the anticancer activity of TP4 in human synovial sarcoma cells and determined the underlying mechanisms. We first demonstrated that TP4 can induce necrotic cell death in human synovial sarcoma AsKa-SS and SW982 cells lines. In addition, we saw that TP4 initiates reactive oxygen species (ROS) production and downregulates antioxidant proteins, such as uncoupling protein-2, superoxide dismutase (SOD)-1, and SOD-2. Moreover, TP4-induced mitochondrial hyperpolarization is followed by elevation of mitochondrial ROS. Calcium overload is also triggered by TP4, and cell death can be attenuated by a necrosis inhibitor, ROS scavenger or calcium chelator. In our experiments, TP4 displayed strong anticancer activity in human synovial sarcoma cells by disrupting oxidative status, promoting mitochondrial hyperpolarization and causing calcium overload.
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