Phytochemicals in Breast Cancer Prevention and Treatment: A Comprehensive Review

Abstract

Extensive investigation has been conducted on plant-based resources for their pharmacological usefulness, including various cancer types. The scope of this review is wider than several studies with a particular focus on breast cancer, which is an international health concern while studying sources of flavonoids, carotenoids, polyphenols, saponins, phenolic compounds, terpenoids, and glycosides apart from focusing on nursing. Important findings from prior studies are synthesized to explore these compounds' sources, mechanisms of action, complementary and synergistic effects, and associated side effects. It was reviewed that the exposure to certain doses of catechins, piperlongumine, lycopene, isoflavones and cucurbitacinfor a sufficient period can provide profound anticancer benefits through biological events such as cell cycle arrest, cells undergoing apoptosis and disruption of signaling pathways including, but not limited to JAK-STAT3, HER2-integrin, and MAPK. Besides, the study also covers the potential adverse effects of these phytochemicals. Regarding mechanisms, the widest attention is paid to Complementary and synergistic strategies are discussed which indicate that it would be realistic to alter the dosage and delivery systems of liposomes, nanoparticles, nanoemulsions, and films to enhance efficacy. Future research directions include refining these delivery approaches, further elucidating molecular mechanisms, and conducting clinical trials to validate findings. These efforts could significantly advance the role of phytocompounds in breast cancer management.

Keywords: anticancer activity; apoptosis; flavonoids; nanotechnology; signaling pathways inhibition; synergistic effects; targeted drug delivery.

Figure 3

Major sources of phytochemicals from food.

Figure 1

Molecular mechanisms of phytochemicals in cancer treatment. It demonstrates their roles in cellular proliferation, apoptosis, and cell cycle. Phytochemicals prevent angiogenesis, metastasis, oxidative stress, and inflammation and regulate redox signaling. They inhibit enzymes, modulate the mammosphere formation, and enhance immune system activity. The anti-apoptotic modulation and targeting of breast cancer cells and preventing the rate of perfusion look positive due to the antioxidative nature of the flavonoids.

Figure 2

Key signaling pathways involved in cancer progression and drug resistance: (A) Akt/PI3K/mTOR Pathway: Growth factors activate receptor tyrosine kinases (RTKs), stimulating PI3K and Akt, leading to mTORC1 activation. This regulates cell growth, proliferation, apoptosis, metastasis, and drug resistance by modulating PTEN expression, miR-21 levels, 4E-BP1, and S6k1. (B) MAPK Pathway: RTK activation triggers RAS, leading to RAF and MEK activation. Downstream effectors (JNK, p38, ERK 1/2) influence similar cellular processes. (C) JAK/STAT Pathway: Cytokines stimulate JAK, phosphorylating STATs, which translocate to the nucleus, driving genes involved in growth and drug resistance.