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Microplastics accumulated in breast cancer patients lead to mitophagy via ANXA2-mediated endocytosis and IL-17 signaling pathway
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Researchers found significant accumulation of microplastics in tissue samples from breast cancer patients and identified the molecular mechanism by which the particles enter cells and cause damage. The microplastics bind to a protein called ANXA2, get absorbed into cells, damage mitochondria (the cell's energy factories), and trigger a self-cleaning process called mitophagy. These findings reveal a specific pathway through which microplastics may contribute to cellular damage in cancer patients.
Breast cancer (BC) is the most common malignancy in women and the leading cause of cancer death. Microplastics (MPs) are plastic fragments with a diameter of less than 5 mm, easily ingested by organisms. Although MPs have been reported to enter the human body through diet, surgery, etc., whether MPs accumulate in BC and their effects have been largely unknown. Our study revealed a significant accumulation of MPs in BC patient samples. MPs pull-down experiments and mass spectrometry (MS) studies showed that MPs bound to annexin A2 (ANXA2) and were endocytosed into cells. This process resulted in mitochondrial damage and subsequent induction of mitophagy. Furthermore, after binding to ANXA2, MPs regulated mitophagy by inhibiting IL-17 exocytosis. These findings revealed the mechanism of toxic effects of MPs in patients with BC, clarified the molecular mechanism of ANXA2-IL-17 signaling pathway causing mitochondrial damage by MPs, and suggested the potential toxic effects and toxicological mechanisms of MPs.
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Disruption of the programmed cell death nexus: potential roles of microplastics and nanoplastics in tumorigenesis
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This review summarizes existing research on how microplastics and nanoplastics, now found in air, water, food and the human body, may contribute to cancer. It describes possible ways these particles disrupt normal cell death processes and carry other chemicals into cells, and notes major gaps that future studies would need to address.
Impact of Environmental Microplastic Exposure on Caco-2 Cells: Unraveling Proliferation, Apoptosis, and Autophagy Activation
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Researchers exposed human intestinal cells to polyethylene and PET microplastics of different sizes and observed significant decreases in cell survival along with increased oxidative stress. The microplastics triggered both programmed cell death (apoptosis) and the cell's self-recycling process (autophagy), with effects varying by particle size. The study suggests that microplastic exposure may compromise the intestinal barrier through multiple pathways of cellular damage.
Mechanism of Nano‐Microplastics Exposure‐Induced Myocardial Fibrosis: DKK3‐Mediated Mitophagy Dysfunction and Pyroptosis
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Researchers investigated how nano-microplastic exposure leads to heart tissue scarring in mice and identified a specific molecular pathway involved. They found that the plastic particles suppressed a protein called DKK3, which disrupted the cell's ability to recycle damaged mitochondria, triggering an inflammatory cell death process that promotes fibrosis. The study reveals a potential mechanism by which long-term microplastic exposure could contribute to cardiac damage.
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