Phytochemical Mechanisms in Cancer Cell Apoptosis

Phytochemicals encompass a diverse array of plant-derived compounds—alkaloids, flavonoids, terpenoids and polyphenols—that exert profound effects on cancer cell fate by engaging apoptotic programmes. Central to their mechanism is the induction of intrinsic apoptosis through mitochondrial membrane permeabilisation, reactive oxygen species (ROS) generation and modulation of Bcl-2 family proteins, as well as activation of death receptor-mediated extrinsic cascades. Key signalling axes such as MAPK, PI3K/AKT, JAK/STAT and NF-κB are targeted directly or indirectly, resulting in caspase activation and cell death. Epigenetic regulation, including histone modification and microRNA expression, further contributes to phytochemical-induced apoptosis and may overcome chemoresistance. These multifaceted actions underpin the global interest in phytochemicals as adjuvant or standalone therapeutic agents, offering potential routes to improve treatment specificity, reduce toxicity and counteract resistant phenotypes in diverse cancer types.

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Phytochemical Mechanisms in Cancer Cell Apoptosis publication trend

The graph below shows the total number of articles in phytochemical mechanisms in cancer cell apoptosis across all publications each year (not limited to Nature Index journals).

Technical terms

Intrinsic apoptosis: A cell-autonomous death programme initiated by mitochondrial outer membrane permeabilisation, leading to caspase activation.

ROS (reactive oxygen species): Highly reactive molecules containing oxygen that can damage cellular components and act as signalling mediators of apoptosis.

c-MET: A receptor tyrosine kinase implicated in cell proliferation and survival, often dysregulated in cancer.

MAPK pathway: Mitogen-activated protein kinase cascade involved in transducing signals that regulate apoptosis, proliferation and differentiation.

Ferroptosis: An iron-dependent form of regulated cell death characterised by lipid peroxidation and distinct from apoptosis.

References

1. Cytostatic Activity of Sanguinarine and a Cyanide Derivative in Human Erythroleukemia Cells Is Mediated by Suppression of c-MET/MAPK Signaling. International Journal of Molecular Sciences (2023).
2. A novel mechanism of 6-methoxydihydroavicine in suppressing ovarian carcinoma by disrupting mitochondrial homeostasis and triggering ROS/ MAPK mediated apoptosis. Frontiers in Pharmacology (2023).
3. Insights on Antitumor Activity and Mechanism of Natural Benzophenanthridine Alkaloids. Molecules (2023).