Molecular Mechanisms of Bioflavonoid Effects in Cancer Therapeutics

Bioflavonoids, a subgroup of natural polyphenolic compounds derived from fruits and vegetables, have attracted considerable attention as potential adjuncts to conventional cancer therapies. These molecules exert pleiotropic effects on malignant cells by modulating key hallmarks of cancer, including proliferation, apoptosis, angiogenesis and metastasis. At the molecular level, bioflavonoids interact with multiple signalling pathways such as the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) cascade, mitogen-activated protein kinase (MAPK) pathways and nuclear factor kappa B (NF-κB) transcriptional activity to induce cell cycle arrest and promote programmed cell death. They can increase intracellular reactive oxygen species, disrupt calcium homeostasis and trigger endoplasmic reticulum stress, culminating in mitochondrial membrane depolarisation and activation of the intrinsic apoptosis pathway. Furthermore, bioflavonoids have been shown to sensitize resistant cancer cells to chemotherapeutic agents, thereby enhancing efficacy and reducing toxic side effects. Preclinical models highlight their capacity to inhibit tumour growth and dissemination through suppression of matrix metalloproteinases, downregulation of anti-apoptotic proteins and upregulation of tumour suppressors such as phosphatase and tensin homologue (PTEN). Their favourable safety profile and multifaceted modes of action position bioflavonoids as promising candidates for combinatorial regimens in precision oncology.

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Molecular Mechanisms of Bioflavonoid Effects in Cancer Therapeutics publication trend

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Technical terms

Bioflavonoid: naturally occurring polyphenolic compounds in plants that modulate cellular signalling pathways.

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

PI3K/AKT pathway: intracellular signalling cascade regulating cell growth, survival and metabolism.

Reactive oxygen species (ROS): highly reactive oxygen-containing molecules that can induce cellular damage or trigger apoptosis.

Endoplasmic reticulum stress: disruption of protein folding homeostasis in the endoplasmic reticulum, leading to activation of stress response pathways.

Cell cycle arrest: interruption of cell cycle progression at specific checkpoints to enable DNA repair or initiate apoptosis.

References

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