Natural Product Cytotoxicity in Cancer Cell Lines

Natural products derived from plants, microorganisms and marine organisms have long served as a reservoir of structurally diverse compounds with potent cytotoxic effects on cancer cell lines. Classes such as alkaloids, terpenoids, flavonoids and polyketides interact with cellular targets to induce programmed cell death, disrupt tumour cell proliferation and overcome multidrug resistance. In vitro screening using assays for half-maximal inhibitory concentration (IC50), cell cycle distribution and markers of apoptosis has revealed that many natural metabolites selectively impair cancer cell viability while sparing non-malignant cells. Mechanistic studies demonstrate that these compounds may trigger intrinsic and extrinsic apoptotic pathways, generate reactive oxygen species, provoke endoplasmic reticulum stress, arrest cells at key points of the cell cycle and engage non-apoptotic death programmes such as necroptosis and anoikis. The breadth of these modes of action underpins global efforts to develop new leads that can complement or synergise with existing chemotherapeutics, addressing the urgent need for more effective and less toxic cancer treatments.

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Natural Product Cytotoxicity in Cancer Cell Lines publication trend

The graph below shows the total number of articles in natural product cytotoxicity in cancer cell lines across all publications each year (not limited to Nature Index journals).

Technical terms

IC50: The concentration of a compound required to inhibit cell viability or a specific biological function by 50% in vitro.

Apoptosis: A form of programmed cell death characterised by caspase activation, DNA fragmentation and membrane blebbing.

Necroptosis: A regulated form of necrotic cell death mediated by RIP kinases and MLKL, independent of caspase activation.

Anoikis: Apoptotic cell death triggered by detachment of cells from the extracellular matrix, preventing metastasis.

Reactive oxygen species (ROS): Chemically reactive molecules containing oxygen, which can damage cellular components and trigger death pathways.

Endoplasmic reticulum stress: A cellular condition arising from accumulation of unfolded proteins, leading to activation of the unfolded protein response and, if unresolved, cell death.

Epithelial–mesenchymal transition (EMT): A process by which epithelial cells acquire mesenchymal traits, enhancing motility and survival; reversal of EMT can sensitise cells to anoikis.

References

1. Apoptosis Induction via ATM Phosphorylation, Cell Cycle Arrest, and ER Stress by Goniothalamin and Chemodrugs Combined Effects on Breast Cancer‐Derived MDA‐MB‐231 Cells. BioMed Research International (2018).
2. Goniothalamin Induces Necroptosis and Anoikis in Human Invasive Breast Cancer MDA-MB-231 Cells. International Journal of Molecular Sciences (2019).
3. Apoptosis Induction, Cell Cycle Arrest and in Vitro Anticancer Activity of Gonothalamin in a Cancer Cell Lines. Asian Pacific Journal of Cancer Prevention (2012).