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6PPDQ promotes the malignant progression of colorectal cancer via enhancing EGF/EGFR signaling
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Tire wear creates a chemical called 6PPD-quinone that washes into waterways and air, and this study found it can make colorectal cancer cells grow, spread, and multiply faster in lab and animal experiments. The chemical works by boosting a cell-growth signal (EGFR) that's already known to drive cancer progression. While this research was done in cells and mice, not humans, it adds to growing concerns that everyday pollution from roads and tires could be a hidden risk factor for cancer, not just an environmental nuisance.
6PPD-quinone (6PPDQ), a transformation product of the rubber antioxidant 6PPD, is a newly identified pollutant found globally. Originating mainly from tire wear particles, it contaminates water bodies, the atmosphere, and the food chain, leading to continuous exposure risks. However, the impact of 6PPDQ on the progression of colorectal cancer remains largely unknown, representing an urgent scientific question to be addressed. This research explored the toxicological impact and molecular mechanisms of 6PPDQ on colorectal cancer. In vitro experiments showed that environmentally relevant concentrations of 6PPDQ significantly promoted proliferation, colony formation, and invasiveness in human colorectal cancer cell lines HCT116 and HT-29, while inducing glycolysis-associated changes marked by elevated lactate production and glucose uptake. Further mechanistic studies indicated that 6PPDQ increased epidermal growth factor receptor (EGFR) expression by stabilizing the transcription factor c-Jun, which activated the EGFR/ERK/AKT signaling pathway; this activation was reversible with the EGFR inhibitor gefitinib. In vivo experiments demonstrated that 6PPDQ exposure accelerated xenograft tumor growth in nude mice and increased EGF/EGFR pathway activity. This study reveals that 6PPDQ promotes colorectal cancer progression via regulating EGF/EGFR signaling, offering new experimental evidence for its environmental health risk assessment. Our research indicates that pollutants from traffic could be environmental risk factors for colorectal cancer, highlighting significant public health and cancer prevention implications.
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Integrated machine learning and experimental validation reveal S6K2 as a key target of 6PPD-quinone in bladder cancer
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Researchers used machine learning across 113 model combinations to identify S6K2 as the key molecular target linking the tire-wear chemical 6PPD-quinone to bladder cancer progression, then confirmed in cell experiments that 6PPD-Q upregulates S6K2 to drive tumor proliferation, migration, and invasion — effects reversed by silencing the gene.
Long‑term exposure of polyethylene nanoplastics promotes colorectal tumorigenesis
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Researchers exposed mice to polyethylene nanoplastics over 66 days and found significantly more colon tumors and heavier tumor burdens compared to controls, with nanoplastics alone triggering colorectal polyps, suggesting these particles promote tumor initiation by disrupting mitochondrial structure and amplifying chronic intestinal inflammation.
Multi-omics analysis and experiments reveal an association between polystyrene microplastics exposure and colorectal cancer progression.
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Scientists found that tiny plastic particles called polystyrene microplastics, commonly found in packaging and everyday plastics, may help colorectal cancer cells grow, spread, and survive in lab and animal studies. This suggests microplastic exposure could play a role in worsening colon cancer, though more research is needed to confirm this happens in humans.
The clinical relevance of microplastic exposure on colorectal cancer: A systematic review
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This systematic review of four studies found that microplastic accumulation in colorectal cancer tissue (25.9-32.2 particles/g) was significantly higher than in healthy controls, with polyamide, polycarbonate, and polypropylene as the most common polymers detected. While a causal relationship has not been established, the evidence points to microplastics as a potential environmental factor in colorectal cancer development.
Effects of microplastics on chemo-resistance and tumorigenesis of colorectal cancer
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For the first time, researchers confirmed the presence of microplastics in human colorectal cancer tissue and showed in animal models that microplastics increased cancer rates and made tumors more resistant to chemotherapy drugs. The study found that microplastics trigger a cell survival mechanism called autophagy that helps cancer cells resist treatment, suggesting plastic pollution could complicate cancer outcomes.
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