Luteolin is widely distributed phytochemical, a flavonoid, in kingdom plantae. Luteolin with potential antioxidant activity prevent ROS‐induced damages and reduce oxidative stress which is mainly responsible in pathogenesis of many diseases. Several chemo preventive activities and therapeutic benefits are associated with luteolin. Luteolin prevents cancer via modulation of numerous pathways, that is, by inactivating proteins; such as procaspase‐9, CDC2 and cyclin B or upregulation of caspase‐9 and caspase‐3, cytochrome C, cyclin A, CDK2, and APAF‐1, in turn inducing cell cycle arrest as well as apoptosis. It also enhances phosphorylation of p53 and expression level of p53‐targeted downstream gene. By Increasing BAX protein expression; decreasing VEGF and Bcl‐2 expression it can initiate cell cycle arrest and apoptosis. Luteolin can stimulate mitochondrial‐modulated functions to cause cellular death. It can also reduce expression levels of p‐Akt, p‐EGFR, p‐Erk1/2, and p‐STAT3. Luteolin plays positive role against cardiovascular disorders by improving cardiac function, decreasing the release of inflammatory cytokines and cardiac enzymes, prevention of cardiac fibrosis and hypertrophy; enhances level of CTGF, TGFβ1, ANP, Nox2, Nox4 gene expressions. Meanwhile suppresses TGFβ1 expression and phosphorylation of JNK. Luteolin helps fight diabetes via inhibition of alpha‐glucosidase and ChE activity. It can reduce activity levels of catalase, superoxide dismutase, and GS4. It can improve blood glucose, insulin, HOMA‐IR, and HbA1c levels. This review is an attempt to elaborate molecular targets of luteolin and its role in modulating irregularities in cellular pathways to overcome severe outcomes during diseases including cancer, cardiovascular disorders, diabetes, obesity, inflammation, Alzheimer's disease, Parkinson's disease, hepatic disorders, renal disorders, brain injury, and asthma. As luteolin has enormous therapeutic benefits, it could be a potential candidate in future drug development strategies.

The continuous progression of cancerous severity due to the interaction of physical (ultraviolet radiation), chemical (smoking, mycotoxins, and heavy metals), and biological (microbial populations) carcinogens inspired scientists to develop a correlation between active therapeutic agents and cancer proliferation. This review highlights the molecular mechanism by which lycopene imparts its anticancerous role, focusing on clinical and animal trials to validate its effectiveness. The antioxidant profile of lycopene promotes anticancerous properties that reduce cancer prevalence by activating cell signaling pathways and gene expression (involved in cancer cell proliferation). Lycopene's anti‐inflammatory properties suppresses the tumor growth and development‐promoting pathways, such as the PI3K/Akt/mTOR pathway. The anticancer property of lycopene is also evidenced by its inhibitory potential of the Wnt/β‐catenin signaling pathway that is involved in cancer cell modulation and propagation. Lycopene also suppresses and neutralizes oxidative stress and reactive oxygen species (ROS)‐induced DNA damage, preventing gene mutation. Inflammation‐induced cell death is mitigated by lycopene's anti‐inflammatory potential that lowers the expression of interleukin 6 (IL‐6) and tumor necrosis factor‐alpha (TNF‐α). Several clinical and randomized control trials have revealed the effect of lycopene supplementation in the management of cancer, including breast cancer, pancreatic cancer, prostate cancer, colon cancer, ovarian cancer, skin cancer, oral cancer, liver cancer, gastric cancer, and kidney cancer, by lessening prostate‐specific antigen (PSA) levels. These studies also accentuate certain limitations that need further trials to evaluate the long‐term consequences of lycopene supplementations and their specific effective dose.

Cancer is a prevalent global disease affecting ~20 million individuals, and this burden causes the death of ~9.7 million people in 2024. The prevalence rate is continuously increasing due to exposure to harmful environmental and occupational contaminants (toxins and chemicals), compromised immune response, genetic modifications, and poor lifestyle and dietary practices. The management of cancer is challenging and demands cost‐effective and safe therapeutic strategies. This review accentuates the anticancer potential of anthocyanins and its associated underlying mechanism. Anthocyanins, the active components extracted from grapes, berries, black chokeberries, eggplants, black currants, sweet cherries, strawberries, black grapes, plums, and red onions, hold antioxidant and anti‐inflammatory potential. The bioavailability of anthocyanins is a crucial factor in imposing their anticancer effect, and this bioavailability can be improved by microbial phenolic catabolites, provision of α‐casein, and nano delivery systems. Anthocyanins hinder cell migration, invasion, and proliferation by inducing apoptosis, suppressing cell cycle at G0/G1, S, or G2/M stages, and modulating signaling pathways such as apoptotic cascades, PI3K/Akt, MAPK, and NF‐κB. Moreover, anthocyanins downregulate oncogenes (Bcl‐2, MYC, and HER2) and improve the activity of tumor suppressor genes (TP53, BRCA1, and RB1). Anthocyanins, particularly cyanidin‐3‐O‐glucoside, suppress inflammation and production of pro‐inflammatory cytokines (COX‐2, TNF‐α, and IL‐6) in colorectal cancer and hepatocellular carcinoma. Moreover, it causes cell cycle inhibition and mitochondrial dysfunction in ovarian and cervical malignancies. Although pre‐clinical studies have proved anticancer activities, further clinical trials are required to validate its therapeutic impact and standard dose regimens.

Isoflavones are currently being investigated by researchers in order to demonstrate their ability to prevent the proliferation of cancer cells. The current review aimed to demonstrate the potential of isoflavones to eliminate cancerous cells in the stomach, liver, lung, breast, and prostate, as their anticancer properties are due to the ability to block the signaling pathways of the extracellular signal‐controlled kinase (MAPK/ERK) and proteasome (PI3K/AKT/mTOR). Isoflavones can inhibit the cell division of various cancer cells. Isoflavones can block the androgen receptor (AR), a protein that is required for the growth and dissemination of prostate cancer. It initiates the caspase cascade and obstructs the production of new proteins to eliminate lung cancer cells. These inhibit colon cancer cells by entering their G2/M cell cycle phase and inducing apoptosis. These are also known to inhibit the production of cyclin‐dependent kinase 2 and cyclin B1, two proteins that are related to an enhanced risk of colon cancer. These suppress the breakdown of cyclin B1 and CDK2 to stop the development of cancer. Preclinical evidence consistently supports the efficacy of isoflavones in suppressing tumor growth; however, human clinical trials show variability due to differences in bioavailability, metabolism, and dosage. Despite their promise as alternative or adjunctive cancer therapies, limitations such as low solubility, interindividual metabolic variations, and inconsistent clinical outcomes necessitate further large‐scale, controlled trials. Future research should focus on improving bioavailability and exploring synergistic effects with conventional therapies.

Human physiology is a complex process encompassing various biochemical mechanisms, regulated by hundreds of chemical mediators, thus making it more complicated to understand. Balance between these mediators is mandatory to continue the helm of life; however, an imbalance can disrupt normal physiological functions and lead to chronic health conditions. Cancer is one such chronic state that occurs due to an imbalance or overproduction of reactive oxygen and nitrogen species (RONS), which are highly unstable and damage other chemical constituents in the body. The mutilation at the cellular level results in DNA and genetic mutation, uncontrolled cell proliferation, metastasis, organ dysfunction, and ultimately mortality. Various types of cancers are intimidating human life globally, and lung cancer is leading them all, followed by breast and colorectal cancer. Oxidative stress (OS) is the main root cause of cancers that occur due to overproduced RONS. Tumor suppressor genes (TSGs) like p53, PTEN, INK4, MADR2, APC, and oncogenes such as HER2, BCR/ABL1, CMYC, EML4AK, RAS, WNT, ERK, and TRK get mutated by OS. Moreover, various pro‐inflammatory markers i.e., IL‐1, IL‐6, TNF‐α, IFN‐γ, TGF‐β and growth factors (VEGF, EGF, IGF‐2) are also involved in cancer progression. Along with these aspects, the oncogenesis involves different signaling pathways/axis such as MAPK, PI3K, mTOR, Wnt/β‐catenin, GSK3, and NF‐κB. Epigallocatechin gallate (EGCG), a bioactive compound abundantly existing in green tea and grapes with strong antioxidant activity and anticancer potential, is a suitable approach to reduce the cancer burden. The in vitro and in vivo anticancer studies of EGCG proved anticancer and anti‐tumor effects through modulation of cancer signaling pathways, reduction in cell proliferation, decreased metastasis, suppressed angiogenesis, enhanced antioxidant activity, inhibited pro‐inflammatory biomarkers, improved TSGs expression, and downregulated oncogenes expression. Shortly, the current review focuses on the anticancer potential of EGCG through possible mechanisms.