Use of Tilapia Hepcidin in Oral Cancer Therapeutics: A Proposal

Abstract

T ilapia hepcidin (TH), an antimicrobial peptide (AMP) derived from tilapia (Oreochromis mossambicus) forms an important component of the fish innate immune defense. 1 However, the functionality of TH is not just limited to its antimicrobial actions, significant applications in cancer research remain an area to be explored. Antimicrobial peptides derived from fish and shrimp demonstrated anticancer activities in addition to their previously discovered antimicrobial action. Three hepcidin-like AMPs can be isolated from tilapia, namely TH1-5, TH2-2, and TH2-3. Of these, TH1-5 and TH2-3 have shown potent antitumor activity. 2 The AMPs from fish exhibit numerous activities that make them promising candidates in cancer therapeutics. The antineoplastic effects of TH are summarized in Flowchart 1. Tilapia hepcidin causes inhibition of tumor cell proliferation. 3 The growth-inhibiting the potential of TH2-3 and TH1-5 is documented in the in vitro studies by Chen et al. 3 and Chang et al. 2 The antineoplastic effect was first shown on human hepatic fibrosarcoma cells. 3 They are also known to prevent tumor invasion and metastasis by affecting cancer cell motility. 4 This characteristic is supposedly due to electrostatic interactions among TH-treated cancer cells, which are not favored due to the neutral charge conferred on healthy cells by zwitterionic nature of their major membrane components such as phosphatidylethanolamine (PE), phosphatidylcholine (PC), and sphingomyelin (SM), and are therefore less attractive to TH2-3 and

Metallated Anticancer Peptides: An Expanded Mechanism that Encompasses Physical and Chemical Bilayer Disruption

“…Another cationic HDP with anti-cancer property, lactoferricin B interacts with the mitochondrial membrane, leading to the formation of ROS and inducing apoptosis 111,112 . Tilapia hepcidins also feature strong anti-cancer activity and the reduction of MDR via a mechanism that involves ROS formation and the activation of a mitochondrial apoptosis pathway [113][114][115][116] .…”