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Quercetin attenuates polyethylene terephthalate nanoplastic-induced malignant phenotypes linked to APOE stabilization and lipid metabolic reprogramming in prostate cancer
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Tiny plastic particles from common plastics (like those in water bottles) can make prostate cancer cells grow, spread, and store more fat by boosting a protein called APOE, essentially giving cancer fuel to progress faster. The good news: quercetin, a natural antioxidant found in foods like onions and apples, reversed these effects in lab and animal studies, suggesting a possible dietary strategy to counteract some harms of plastic exposure. More research is needed before this translates into human treatment, but it's an encouraging early clue linking everyday plastic pollution, diet, and cancer risk.
Micro- and nanoplastics (MNPs) are emerging environmental contaminants with increasing evidence of biological activity in mammalian systems. However, the molecular mechanisms by which chronic polyethylene terephthalate nanoplastic (PET-NPs) exposure promotes prostate cancer progression, and whether this process can be attenuated by quercetin, remain poorly understood. DU-145 and LNCaP cells were subjected to repeated PET-NPs exposure and analyzed using functional assays, DIA proteomics, protein-stability and ubiquitination assays, APOE loss- and gain-of-function experiments, and xenograft models. PET-NPs enhanced proliferation, migration, invasion, intracellular lipid accumulation, and tumor growth. Proteomic analysis highlighted cholesterol metabolism, lipid transport, and PI3K/AKT signaling, leading to prioritization of APOE. PET-NPs increased APOE protein abundance without altering APOE mRNA, prolonged APOE protein stability, and reduced its ubiquitination-dependent proteasomal turnover. APOE knockdown attenuated PET-NPs-induced increases in triglyceride and total cholesterol levels, PIK3CA expression, AKT phosphorylation, proliferation, migration, and invasion, supporting APOE as an important but non-exclusive functional contributor. Quercetin reduced APOE mRNA and protein abundance and suppressed PET-NPs-associated lipid accumulation, PI3K/AKT activation, and malignant phenotypes in vitro. APOE overexpression partially restored PIK3CA expression, AKT phosphorylation, total cholesterol levels, EdU incorporation, invasion, and migration in both DU-145 and LNCaP cells under PET-NPs plus quercetin treatment, whereas the restoration of triglyceride levels reached statistical significance only in LNCaP cells. In vivo, quercetin attenuated PET-NPs-associated subcutaneous and orthotopic tumor progression and reduced APOE, p-AKT, PLIN2, Ki-67, and MMP2 staining. These findings indicate that APOE contributes to, but does not fully account for, the inhibitory effects of quercetin.
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Microplastic-associated pollutants in prostate carcinogenesis and plant-based chemo-preventive strategies
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Researchers reviewed evidence that microplastics accumulate in prostate tissue at higher concentrations in malignant than benign samples and act as carriers for endocrine disruptors including bisphenols, phthalates, and PFAS, proposing that androgen receptor disruption, oxidative stress, and chronic inflammation form a plausible toxicity triad linking MP exposure to prostate carcinogenesis.
Microplastics and prostate cancer.
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Scientists found tiny plastic particles called microplastics in prostate tissue from 9 out of 10 men with prostate cancer, with higher amounts in cancerous tissue compared to healthy tissue. While this small study doesn't prove that microplastics cause cancer, it suggests these particles from everyday plastic items may accumulate in our bodies and could potentially play a role in disease. More research is needed to understand if microplastics truly increase cancer risk or if they're just more likely to build up in already-diseased tissue.
Quercetin intervention mitigates small intestinal damage and immunologic derangement induced by polystyrene nanoplastics: Insights from multi-omics analysis in mice
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Researchers found that quercetin, a natural compound found in fruits and vegetables, protected mice from gut damage and immune system disruption caused by polystyrene nanoplastics. The nanoplastics damaged the small intestine and disrupted immune balance, but quercetin reversed much of this harm by restoring healthy gut bacteria and gene activity. This suggests that dietary compounds like quercetin might help counteract some negative health effects of nanoplastic exposure.
Exploration of potential targets and toxicological mechanisms of microplastic exposure-induced osteoarthritis based on network toxicology, molecular docking and experimental validation
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Scientists found that tiny plastic particles (microplastics), which we regularly ingest through food and air, may damage joint cartilage and contribute to osteoarthritis by disrupting specific genes involved in inflammation and cell damage. Using computer modeling and lab experiments on cartilage cells, researchers also found that quercetin—a natural compound found in fruits and vegetables—may help protect against this damage, though more research is needed before it could be recommended as a treatment. This study adds to growing concerns about how everyday plastic exposure might affect joint health, while pointing toward a possible natural way to help defend against it.
Polyethylene terephthalate micro-/nanoplastics suppress SAT1-dependent ferroptosis in triple-negative breast cancer
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Scientists found tiny plastic particles from PET (a common plastic used in bottles and packaging) inside human breast cancer tissue, and discovered these particles may help aggressive "triple-negative" breast cancer cells survive and grow faster. The plastic appears to block a natural cell-death process that normally helps kill off cancer cells, essentially giving tumors a survival advantage. While this research was done in cells and mice, it adds to growing evidence that the microplastics we're exposed to daily may not just be inert particles passing through our bodies, they could actively influence cancer progression.
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