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Marine Antimicrobial Peptide TP4 Exerts Anticancer Effects on Human Synovial Sarcoma Cells via Calcium Overload,

Bor-Chyuan Su1, Giun-Yi Hung2,3, Yun-Chieh Tu4

  • 1Department of Anatomy and Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.

Marine Drugs
|February 10, 2021
PubMed

Insights

Tilapia piscidin 4 (TP4) shows promise as an anticancer agent for synovial sarcoma. This marine peptide induces cell death by disrupting the oxidative status, mitochondrial function, and calcium balance in cancer cells.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Synovial sarcoma is an aggressive soft-tissue cancer with high metastatic rates and limited treatment options.
  • Existing therapies for metastatic synovial sarcoma are often ineffective, highlighting the need for novel therapeutic agents.
  • Marine antimicrobial peptides, such as Tilapia piscidin 4 (TP4), possess diverse biological activities, including anticancer potential.

Purpose of the Study:

  • To evaluate the anticancer activity of Tilapia piscidin 4 (TP4) against human synovial sarcoma cells.
  • To elucidate the underlying molecular mechanisms responsible for TP4's cytotoxic effects in synovial sarcoma.

Main Methods:

  • Assessed TP4's cytotoxic effects on human synovial sarcoma cell lines (AsKa-SS and SW982).
  • Investigated TP4-induced changes in reactive oxygen species (ROS) production and antioxidant protein levels (UCP-2, SOD-1, SOD-2).
  • Analyzed TP4's impact on mitochondrial membrane potential, mitochondrial ROS, and intracellular calcium levels.
  • Utilized necrosis inhibitors, ROS scavengers, and calcium chelators to confirm the cell death pathway.

Main Results:

  • TP4 demonstrated significant necrotic cell death induction in both synovial sarcoma cell lines.
  • TP4 treatment led to increased ROS production and downregulation of key antioxidant proteins.
  • TP4 triggered mitochondrial hyperpolarization, elevated mitochondrial ROS, and caused calcium overload.
  • Inhibition of necrosis, ROS, or calcium overload attenuated TP4-induced cell death, confirming the mechanism.

Conclusions:

  • TP4 exhibits potent anticancer activity against human synovial sarcoma cells.
  • The mechanism involves disruption of cellular oxidative status, mitochondrial dysfunction, and calcium dysregulation.
  • TP4 represents a potential novel therapeutic candidate for treating metastatic synovial sarcoma.
Keywords:
TP4calcium overloadhuman synovial sarcomamarine antimicrobial peptidemitochondria

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