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61,005 resultsShowing papers similar to DEHP mediates drug resistance by metabolic reprogramming in colorectal cancer cells
ClearMicroplastics promote chemoresistance by mediating lipid metabolism and suppressing pyroptosis in colorectal cancer
This study found that microplastics can make colorectal cancer cells more resistant to chemotherapy drugs. Cancer cells absorb microplastics through a protein called clathrin, which triggers increased fat absorption and suppresses a cell death pathway that drugs normally rely on. These findings suggest that microplastic accumulation in the gut could potentially interfere with cancer treatment effectiveness.
Effects of microplastics on chemo-resistance and tumorigenesis of colorectal cancer
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.
In vitro evidence and integrative bioinformatics identify the SGLT2-PPARγ axis as a target against polyethylene microplastic-driven metabolic reprogramming in colorectal cancer cells
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.
Microplastic accumulation in endometrial cancer tissues and its metabolic impact
Researchers examined microplastic levels in endometrial cancer tissues compared to normal tissue and found that cancer tissues contained significantly higher concentrations of plastic particles. The most common plastics detected were polyethylene, polypropylene, and polystyrene. Metabolic analysis revealed that microplastic presence was associated with changes in cancer-related metabolic pathways, suggesting that microplastics may play a role in promoting tumor development through metabolic reprogramming.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
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.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
Combining network toxicology, machine learning, and molecular docking, this study found that PET plastic degradation products ethylene glycol and terephthalic acid may influence colorectal cancer prognosis through 43 shared genes linked to TNF/IL-17 signaling and glucocorticoid-mediated 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
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.
Impact of Plastic-Related Compounds on P-Glycoprotein and Breast Cancer Resistance Protein In Vitro
Researchers examined how plastic-related compounds affect P-glycoprotein and breast cancer resistance protein in vitro, finding that plasticizers and plastic additives can inhibit these critical cellular defense transporters involved in detoxification.
Identification and analysis of microplastics in peritumoral and tumor tissues of colorectal cancer
Researchers examined tumor and surrounding tissue from colorectal cancer patients and found a diverse range of microplastics, including PVC and polyethylene, with tumor tissues containing a greater variety and higher distribution of microplastics than adjacent healthy tissue. A protein called clathrin that helps cells absorb materials was highly active in the cancer tissue, suggesting it may facilitate microplastic uptake and pointing to a potential link between microplastic exposure and colorectal cancer development.
Polystyrene nanoplastics promote colitis-associated cancer by disrupting lipid metabolism and inducing DNA damage
In a mouse study, polystyrene nanoplastics accelerated the development of colon cancer linked to inflammatory bowel disease by disrupting fat metabolism and causing DNA damage in intestinal cells. The nanoplastics also altered gut bacteria and increased intestinal inflammation, suggesting that plastic particle exposure could worsen outcomes for people already at risk for colon cancer.
Cell Specific Metabolomic and Fluxomic Responses to Polylactic Acid Nanoplastics Exposure in Human Intestinal Cells
Metabolomic and fluxomic analysis of human intestinal cells (Caco-2 and HT29-MTX) exposed to PLA nanoplastics revealed cell-type-specific metabolic reprogramming, with changes in glycolysis, TCA cycle flux, and amino acid metabolism suggesting altered energy handling in intestinal epithelium.
Microplastics role in cell migration and distribution during cancer cell division
Researchers exposed human colorectal cancer cells to polystyrene micro- and nanoplastics and found the particles persisted inside cells without being eliminated, were passed from parent to daughter cells during division, and significantly increased cell migration -- a key step in cancer spreading. These findings suggest microplastics could act as hidden promoters of tumor progression in the gut, where plastic exposure through food is highest.
A review of environmental metabolism disrupting chemicals and effect biomarkers associating disease risks: Where exposomics meets metabolomics
This review examines how environmental chemicals, including contaminants associated with plastics, can disrupt human metabolism and contribute to conditions like obesity and diabetes. Researchers mapped the connections between chemical exposure and changes in metabolic biomarkers that signal disease risk. The study highlights the emerging field of metabolism-disrupting chemicals and the importance of understanding how everyday environmental exposures influence long-term metabolic health.
Microbiology combined with metabonomics revealing the response of soil microorganisms and their metabolic functions exposed to phthalic acid esters
Researchers examined how common plastic plasticizers (phthalic acid esters) affect soil microorganisms and their metabolic functions using genomic sequencing and metabolomics. They found that while plasticizers did not significantly change bacterial diversity in the short term, they altered community structure and disrupted metabolic pathways, with dibutyl phthalate affecting 172 metabolites and 43 metabolic pathways. The study also identified certain soil bacteria with potential to degrade these plasticizer compounds.
Polyvinyl chloride microplastics exposure accelerates endometrial cancer progression via regulating AHR/CYP1A1 signaling pathway
Scientists found that tiny plastic particles from PVC (a common type of plastic) can make endometrial cancer grow and spread faster in lab studies using human cells and mice. This matters because PVC microplastics are everywhere in our environment - from food packaging to water bottles - and endometrial cancer rates are rising in women. The research suggests that reducing exposure to plastic particles could be important for preventing this type of cancer.
Di-(2-ethylhexyl) phthalate and its metabolites research trend: a bibliometric analysis
This bibliometric analysis mapped research trends on di-(2-ethylhexyl) phthalate (DEHP) and its metabolites, identifying growth areas, major contributors, and gaps in understanding human exposure, metabolism, and health effects of this common plasticizer.
Microplastic changes during the development of cervical cancer and its effects on the metabolomic profiles of cancer tissues
Researchers found microplastics in cervical cancer tissue, with polyethylene and polypropylene being the most common types, and levels increased as the cancer progressed to more advanced stages. The microplastics appeared to alter the chemical environment within the cancer tissue, suggesting they may play a role in how cervical cancer develops, though more research is needed to confirm a causal link.
Polystyrene micro and nano-particles induce metabolic rewiring in normal human colon cells: A risk factor for human health
Researchers exposed normal human colon cells to polystyrene micro and nanoplastic particles and observed significant metabolic changes in the cells. The study found that these plastic particles altered energy metabolism and cellular pathways in ways that could increase vulnerability to disease. These findings raise concerns that routine ingestion of microplastics through contaminated food may affect normal intestinal cell function in humans.
DEHP chronic exposure disturbs the gut microbial community and metabolic homeostasis: Gender-based differences in zebrafish
Chronic exposure of zebrafish to DEHP — a phthalate plasticizer found in many plastic products — from embryo to adulthood disrupted gut microbial communities and metabolic balance, with effects that differed between males and females. This suggests that phthalate exposure from plastic products may alter gut health and metabolism in ways that could be relevant to human health.
Impact of a Modified Fenton Process on the Degradation of a Component Leached from Microplastics in Bottom Sediments
Researchers tested a modified chemical process (Fenton reaction) for breaking down di(2-ethylhexyl) phthalate (DEHP), a plasticizer that leaches from microplastics into sediments. The process showed promising results for degrading this hard-to-remove contaminant, which is associated with hormone disruption.
Tumour-infiltrating microplastics disrupt the JAK-STAT-microbiota axis to promote immunotherapy resistance in colorectal cancer
Researchers isolated microplastics from colorectal cancer tumor tissues and blood samples and examined their properties and effects on cancer progression. They found that tumor-infiltrating microplastics disrupted the JAK-STAT signaling pathway and altered gut microbiota composition, potentially reducing the effectiveness of immunotherapy. The study suggests that microplastic presence in tumors may be a factor worth investigating in cancer treatment outcomes.
Why Is Colorectal Cancer Occurring Earlier? Metabolic Dysfunction, Underrecognized Carcinogens, and Emerging Controversies
Researchers reviewed the rising incidence of early-onset colorectal cancer in people under 50, synthesizing epidemiological, molecular, and multi-omics evidence that implicates metabolic dysfunction, accelerated epigenetic aging, gut microbiome dysbiosis, and modern environmental exposures including micro- and nanoplastics as converging contributors to this trend.
Effect of paclitaxel octreotide conjugate on human ovarian paclitaxel-resistant cell xenograft tumor model and the mechanism underlying reversal of paclitaxel resistance
This paper is not relevant to microplastics — it examines the efficacy of a paclitaxel-octreotide conjugate for overcoming drug resistance in human ovarian cancer cell xenograft models.
Effects of prenatal exposure to phthalates and Hexamoll® DINCH derived from urinary untargeted metabolomics analysis
This study examined how prenatal exposure to phthalates and their substitute DINCH—chemicals used as plasticizers in plastic products—affected metabolic processes in children. Metabolomics analysis revealed biological changes linked to plasticizer exposure, raising concerns about effects on early childhood development.