Abstract
Temporin-1CEa is an antimicrobial peptide isolated from the skin secretions of the Chinese brown frog (Rana chensinensis). We have previously reported the rapid and broad-spectrum anticancer activity of temporin-1CEa in vitro. However, the detailed mechanisms for temporin-1CEa-induced cancer cell death are still weakly understood. In the present study, the mechanisms of temporin-1CEa-induced rapid cytotoxicity on two human breast cancer cell lines, MDA-MB-231 and MCF-7, were investigated. The MTT assay and the LDH leakage assay indicated that one-hour of incubation with temporin-1CEa led to cytotoxicity in a dose-dependent manner. The morphological observation using electronic microscopes suggested that one-hour exposure of temporin-1CEa resulted in profound morphological changes in both MDA-MB-231 and MCF-7 cells. The membrane-disrupting property of temporin-1CEa was further characterized by induction of cell-surface exposure of phosphatidylserine, elevation of plasma membrane permeability and rapid depolarization of transmembrane potential. Moreover, temporin-1CEa evoked intracellular calcium ion and reactive oxygen species (ROS) elevations as well as collapse of mitochondrial membrane potential (Δφm). In summary, the present study indicates that temporin-1CEa triggers rapid cell death in breast cancer cells. This rapid cytotoxic activity might be mediated by both membrane destruction and intracellular calcium mechanism.
Highlights
Numerous chemotherapeutic agents have been developed for cancer treatment, including antimetabolites, DNA alkylating drugs, and hormone agonists/antagonists
Temporin-1CEa Induces Breast Cancer Cell Death As shown in Fig. 1, both MTT assay and lactate dehydrogenase (LDH) leakage assay indicated that treatment of cancer cells with temporin-1CEa induced cell death in a concentration-dependent manner
The in vitro cytotoxicity assay indicated that MCF-7 cancer cells were more vulnerable to the temporin-1CEa-induced cytotoxicity than MDA-MB-231 cells
Summary
Numerous chemotherapeutic agents have been developed for cancer treatment, including antimetabolites, DNA alkylating drugs, and hormone agonists/antagonists. Antimicrobial peptides (AMPs, termed host defense peptides) have been shown to exert potent antitumor effects both in vitro and in vivo and received attention as new class anticancer molecules [2,3,4,5]. These peptides have several advantages over currently used anticancer therapeutics, such as selective cytotoxicity for cancer cells, bypass of the multidrug-resistance mechanism, and synergism effects in combination therapy [6]. Besides the direct membrane-destructing effect, some researchers have suggested that AMPs might exert cytolytic activity against cancer cells through ion-permeable channel formation in the cell membrane [13] or other non-membranolytic intracellular actions [14,15,16]
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