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Updated: May 27, 2026

Evaluation of Caspase Activation to Assess Innate Immune Cell Death
Published on: January 20, 2023
Pardaxin, an antimicrobial peptide, triggers caspase-dependent and ROS-mediated apoptosis in HT-1080 cells
Tsui-Chin Huang1, Jheng-Fong Lee1, Jyh-Yih Chen1
1Marine Research Station, Institute of Cellular and Organismic Biology, Academia Sinica, 23-10 Dahuen Rd., Jiaushi, Ilan 262, Taiwan.
Abstract:
Pardaxin is an antimicrobial peptide (AMP) that was first isolated from secretions of the Red Sea Moses sole. The role of pardaxin in inducing apoptosis for preventing cancer has not yet been investigated. In the present study, we examined the antitumor activity of pardaxin against human fibrosarcoma HT-1080 cells; pardaxin inhibited cell proliferation by inducing apoptosis, as demonstrated by an increase in the externalization of plasma membrane phosphatidylserine and the presence of chromatin condensation. Additionally, pardaxin-treated cells showed elevation of caspase-3/7 activities, disruption of the mitochondrial membrane potential, and accumulation of reactive oxygen species (ROS) production. Inhibition of ROS production and caspase-3/7 activities reduced pardaxin-induced effects. Taken together, these findings suggest that pardaxin may be a potential anticancer agent for selectively inducing apoptosis in cancer cells.
Insights
Pardaxin, an antimicrobial peptide, shows potential as an anticancer agent by inducing apoptosis in human fibrosarcoma cells. This peptide selectively triggers programmed cell death, offering a novel approach for cancer treatment.
Area of Science:
- Biochemistry
- Molecular Biology
- Pharmacology
Background:
- Antimicrobial peptides (AMPs) are being explored for therapeutic applications.
- Pardaxin, isolated from the Red Sea Moses sole, is an AMP with unknown anticancer properties.
- Apoptosis induction is a key mechanism in cancer prevention.
Purpose of the Study:
- To investigate the antitumor activity of pardaxin against human fibrosarcoma HT-1080 cells.
- To determine if pardaxin induces apoptosis and explore the underlying mechanisms.
- To evaluate pardaxin's potential as a novel anticancer agent.
Main Methods:
- Cell proliferation assays were performed on HT-1080 cells treated with pardaxin.
- Apoptosis was assessed by measuring phosphatidylserine externalization and chromatin condensation.
- Caspase-3/7 activities, mitochondrial membrane potential, and reactive oxygen species (ROS) production were analyzed.
Main Results:
- Pardaxin significantly inhibited HT-1080 cell proliferation by inducing apoptosis.
- Apoptosis was evidenced by increased phosphatidylserine externalization and chromatin condensation.
- Pardaxin elevated caspase-3/7 activities, disrupted mitochondrial membrane potential, and increased ROS production, which were crucial for its effects.
Conclusions:
- Pardaxin exhibits significant antitumor activity against human fibrosarcoma cells.
- The mechanism involves pardaxin-induced apoptosis, mediated by caspase-3/7 activation and ROS generation.
- Pardaxin represents a promising candidate for developing targeted cancer therapies.
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