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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.
Environmental polyethylene terephthalate micro- and nanoplastics (PET-MNPs) are biologically accessible contaminants, but their effects on clear cell renal cell carcinoma (ccRCC) progression remain unclear. Using 786-O and CAKI-1 cells and subcutaneous and orthotopic xenograft models, we found that PET-MNP exposure enhanced malignant phenotypes and tumor growth, accompanied by increased intracellular and mitochondrial ROS. Mitochondrial superoxide accumulation was associated with membrane depolarization, reduced ATP levels, ultrastructural abnormalities, and decreased SOD2 expression and Mn-SOD activity. Mechanistically, PET-MNP exposure increased AKT and inhibitory GSK3β Ser9 phosphorylation, reduced degradation-associated phosphorylation and ubiquitination of β-catenin, and enhanced β-catenin stability, nuclear accumulation, and transcriptional activity. Time-course analysis indicated that AKT activation preceded prominent GSK3β and β-catenin changes. MitoTEMPO, pharmacological AKT or β-catenin inhibition, AKT knockdown, β-catenin-S33Y rescue, and GSK3β-S9A experiments further supported the functional involvement of mitochondrial ROS-associated AKT/GSK3β/β-catenin regulation. ChIP-qPCR and RT-qPCR showed increased β-catenin recruitment to MYC and CCND1 regulatory regions and enhanced transcription. These findings support a role for mitochondrial ROS-associated AKT/GSK3β/β-catenin regulation in PET-MNP-promoted ccRCC progression.
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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.
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