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In vitro evidence and integrative bioinformatics identify the SGLT2-PPARγ axis as a target against polyethylene microplastic-driven metabolic reprogramming in colorectal cancer cells
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Researchers used in vitro experiments and bioinformatics to identify the SGLT2-PPARgamma axis as a molecular target affected by polyethylene microplastic exposure in colorectal cancer cells. The study suggests that microplastics may influence metabolic reprogramming in cancer cells, highlighting a potential interplay between environmental pollutants and metabolic regulation.
Results unveil the adverse effects of PE on CRC progression underscoring a dynamic interplay between environmental pollutants, metabolic regulators and dietary bioactive modulators. This evidence lay the groundwork for future studies on integrative approaches aimed at mitigating the effects of microplastic pollution on CRC.
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This computational study investigated how PET microplastic degradation products affect colorectal cancer prognosis, identifying 43 genes linking ethylene glycol and terephthalic acid exposure to cancer pathogenesis via chronic inflammation mediated through TNF/IL-17 and glucocorticoid metabolic pathways.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
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Researchers used network toxicology, machine learning, and molecular docking to investigate how PET degradation products—ethylene glycol and terephthalic acid—affect colorectal cancer prognosis through the glucocorticoid signaling pathway. The analysis identified 43 shared target genes, suggesting that PET breakdown products may worsen colorectal cancer outcomes by dysregulating glucocorticoid-mediated anti-inflammatory and cell survival signals.
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