Tea tree oil extract causes mitochondrial superoxide production and apoptosis as an anticancer agent, promoting tumor infiltrating neutrophils cytotoxic for breast cancer to induce tumor regression.

Autor: Clark AM; School of Pharmacy and Medical Science, Menzies Health Institute of Queensland, Griffith University, Gold Coast Campus, Southport, Queensland 4222, Australia., Magawa C; School of Pharmacy and Medical Science, Menzies Health Institute of Queensland, Griffith University, Gold Coast Campus, Southport, Queensland 4222, Australia., Pliego-Zamora A; School of Pharmacy and Medical Science, Menzies Health Institute of Queensland, Griffith University, Gold Coast Campus, Southport, Queensland 4222, Australia., Low P; School of Pharmacy and Medical Science, Menzies Health Institute of Queensland, Griffith University, Gold Coast Campus, Southport, Queensland 4222, Australia., Reynolds M; School of Pharmacy and Medical Science, Menzies Health Institute of Queensland, Griffith University, Gold Coast Campus, Southport, Queensland 4222, Australia; Australian Botanical Bioscience Pty. Ltd., Australia., Ralph SJ; School of Pharmacy and Medical Science, Menzies Health Institute of Queensland, Griffith University, Gold Coast Campus, Southport, Queensland 4222, Australia. Electronic address: s.ralph@griffith.edu.au.
Jazyk: angličtina
Zdroj: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie [Biomed Pharmacother] 2021 Aug; Vol. 140, pp. 111790. Date of Electronic Publication: 2021 Jun 11.
DOI: 10.1016/j.biopha.2021.111790
Abstrakt: The antitumor activity of the tea tree oil (TTO) derived product, Melaleuca Alternifolia Concentrate (MAC) was characterized mechanistically at the molecular and cellular level. MAC was analyzed for its anticancer activity against human prostate (LNCaP) and breast (MCF-7) cancer cell lines growing in vitro. MAC (0.02-0.06% v/v) dose-dependently induced the intrinsic (mitochondrial) apoptotic pathway in both the LNCaP and MCF-7 cell lines, involving increased mitochondrial superoxide production, loss of mitochondrial membrane potential (MMP), caspase 3/7 activation, as well as the presence of TUNEL + and cleaved-PARP + cell populations. At concentrations of 0.01-0.04% v/v, MAC caused cell cycle arrest in the G 0/1 -phase, as well as autophagy. The in vivo anticancer actions of MAC were examined as a treatment in the FVB/N c-Neu murine model for spontaneously arising breast cancers. Intratumoral MAC injections (1-4% v/v) significantly suppressed tumor progression in a dose-dependent manner and was associated with greater levels of tumor infiltrating neutrophils exhibiting anticancer cytotoxic activity. Induction of breast cancer cell death by MAC via the mitochondrial apoptotic pathway was also replicated occurring in tumors treated in vivo. In conclusion, our data highlights the potential for the Melaleuca-derived MAC product inducing anticancer neutrophil influx, supporting its application as a novel therapeutic agent.
(Crown Copyright © 2021. Published by Elsevier Masson SAS. All rights reserved.)
Databáze: MEDLINE
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