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NOX4-related ROS couples PET micro- and nanoplastic exposure to JAK2/STAT3 activation in clear cell renal cell carcinoma
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In lab experiments and mice, tiny plastic particles from PET (a common plastic) sped up the growth and spread of kidney cancer cells. The particles raised levels of a cell-damaging molecule called ROS, which triggered a chain of chemical signals inside cells linked to tumor growth.
The potential influence of polyethylene terephthalate micro- and nanoplastics (PET-MNPs) on the progression of clear cell renal cell carcinoma (ccRCC) remains insufficiently defined. In this study, environmentally derived PET-MNPs promoted ccRCC cell growth, clonogenic capacity, migration, and invasion, and also accelerated tumor development in subcutaneous and orthotopic models. PET-MNP exposure markedly elevated intracellular ROS and H₂O₂ and preferentially increased NOX4 among the NOX family members examined. Silencing NOX4 attenuated ROS and H₂O₂ accumulation and weakened the associated malignant phenotypes both in vitro and in vivo. Functional rescue further showed that wild-type NOX4, but not the catalytically impaired NOX4-P437H mutant, reinstated oxidative signaling and JAK2/STAT3 activation after NOX4 depletion. Transcriptomic analysis of PET-MNP-responsive genes reversed by NOX4 knockdown highlighted JAK-STAT signaling, which was subsequently narrowed to the JAK2/STAT3 branch by protein screening. JAK2 depletion impaired STAT3 Tyr705 phosphorylation, nuclear localization, and transcriptional activity, whereas STAT3 silencing suppressed PET-MNP-induced tumor-promoting phenotypes. Conversely, constitutively active STAT3 partially restored the effects lost after NOX4 depletion. These results define a NOX4-related ROS-JAK2/STAT3 signaling cascade that contributes to PET-MNP-driven ccRCC progression.
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Environmental Polyethylene Terephthalate Micro‐ and Nanoplastics Promote Clear Cell Renal Cell Carcinoma Progression Through Mitochondrial ROS‐Associated AKT/GSK3β/β‐Catenin Signaling
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Tiny plastic particles from PET (the plastic used in water bottles and food packaging) may fuel the growth of kidney cancer cells, according to a new study using cancer cells and mice. The researchers found these microplastics cause stress inside cell "power plants" (mitochondria), which then flips on a chain of signals that helps cancer cells grow and spread faster. While this doesn't prove microplastics cause cancer in people, it adds to growing evidence that these ubiquitous particles may not be as harmless as once thought, especially for someone already dealing with cancer.
Nanoplastic uptake through ROS-induced plasma membrane damage exacerbates renal fibrosis under hypoxia
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In mice, low oxygen levels in the kidney (a condition common in kidney disease) caused tiny plastic particles to build up more easily and worsen kidney damage and scarring, while plastic exposure alone caused no harm. This suggests people with reduced kidney blood flow or oxygen, such as those with existing kidney problems, may be more vulnerable to health effects from nanoplastic pollution.
Multimodal detection and analysis of microplastics in human clear cell renal cell carcinoma
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Researchers used multiple detection methods to analyze microplastics in tumor and normal kidney tissue from patients with clear cell renal cell carcinoma. They found that tumor tissues contained significantly higher levels of total microplastics, particularly polyethylene and PVC, compared to surrounding normal tissue. Gene expression analysis revealed that patients with higher microplastic levels showed activation of signaling pathways associated with tumor progression, suggesting a potential link worth further investigation.
Polystyrene Microplastics Exposure Aggravates Clear Cell Renal Cell Carcinoma Progression via the NF‐κB and TGF‐β Signaling Pathways
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Researchers detected polystyrene microplastics in clear cell renal cell carcinoma tissue samples and showed in cell culture and animal models that microplastic exposure aggravated cancer progression by activating NF-κB and TGF-β signaling pathways that promote tumor growth and spread.
Polyethylene terephthalate nanoplastics promote gastric cancer progression by inhibiting the TNF-α/JAK1/STAT1 signaling pathway and shaping an immunosuppressive microenvironment
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Tiny plastic particles from PET plastic (commonly used in bottles and food packaging) may do more than just contaminate our bodies—new research in mice and lab-grown cells shows they can actually help stomach cancer grow faster and resist chemotherapy. These nanoplastics appear to weaken the immune system's ability to fight tumors and block a key cancer-suppressing pathway in the body. While this study was done in mice and cells rather than humans, it adds to growing evidence that chronic exposure to microplastics isn't just an environmental issue—it could be a real risk factor for cancer progression.
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