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Chronic nanoplastics exposure drives lung cancer progression through ATF3/PCK2 axis-mediated rewiring of truncated gluconeogenesis
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Researchers found that prolonged exposure of lung cancer cells to environmentally relevant nanoplastic doses accelerates tumor progression by activating an ER stress pathway that upregulates the ATF3-PCK2 metabolic axis, rewiring cancer cell metabolism toward anabolic gluconeogenesis — identifying nanoplastics as potential environmental tumor promoters.
Environmental factors are critical for lung cancer progression, and nanoplastics (NPs) pose evolving health risks. Due to small size, NPs are readily inhaled and accumulate in lung tissues, but their long-term impact on lung cancer remains unclear. This study used long-term cell culture and orthotopic lung cancer models exposed to environmentally relevant NPs doses to investigate oncogenic potentials. Our results show that prolonged NPs exposure enhances lung adenocarcinoma A549 cell proliferation, migration, and invasion in vitro and accelerates lung tumor progression in vivo. Transcriptomic analysis identified activating transcription factor-3 (ATF3), induced by the protein kinase RNA-like ER kinase (PERK) branch of the unfolded protein response (UPR) and endoplasmic reticulum stress (ERs), as a key driver. Mechanistically, ATF3 activation upon NPs exposure promotes cancer progression by upregulating mitochondrial phosphoenolpyruvate carboxykinase (PCK2), a rate-limiting enzyme in truncated gluconeogenesis and serine/glycine biosynthesis. The ATF3-PCK2 axis facilitates metabolic reprogramming through enhanced anabolic gluconeogenesis, promoting lung cancer malignant progression under NPs exposure. These findings establish NPs as environmental tumor promoters in lung cancer and elucidate a novel metabolic activation pathway underlying their oncogenic effects, providing mechanistic insights with implications for risk assessment, prevention, and therapeutic intervention.
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Researchers found that long-term exposure to polystyrene nanoplastics promoted lung cancer cell growth and migration by reprogramming cellular metabolism. The study suggests nanoplastics activate a specific metabolic pathway through the stress-response protein ATF3, shifting energy production in ways that enhance cancer cell proliferation.
Long-TermExposure to Real-Life Polyethylene TerephthalateNanoplastics Induces Carcinogenesis In Vitro
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Long-term in vitro exposure of lung epithelial cells to real-life PET nanoplastics — particles collected from the environment rather than synthesized models — induced carcinogenic transformation including anchorage-independent growth and epithelial-to-mesenchymal transition, suggesting that chronic inhalation exposure to PET nanoplastics may contribute to lung cancer risk.
Nuclear accumulation of stabilized SPDEF drives nanoplastic-induced lung adenocarcinoma progression through sustaining inflammation via TRIB3–c-Fos signaling
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Scientists exposed lung cancer cells and mice to nanoplastics (tiny plastic particles from broken-down plastic pollution) at levels similar to what people might realistically encounter, and found that long-term exposure sped up lung tumor growth. They traced this to a chain reaction inside cells—a protein called SPDEF builds up and triggers ongoing inflammation—that appears to fuel cancer progression. While this research was done in cells and mice rather than humans, it adds to growing evidence that everyday plastic pollution exposure may carry real cancer-related risks worth taking seriously.
Polystyrene nanoplastics and lung cancer: Insights from network toxicology and mechanistic in vitro studies
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Network toxicology analysis identified 189 potential molecular targets linking polystyrene nanoplastic exposure to lung cancer pathways, and in vitro experiments confirmed that nanoplastics promote lung cancer cell proliferation and resistance to apoptosis via PI3K/AKT signaling.
Personalized Pathogenic Nanoplastic Coronas Orchestrate Efferocytosis-Driven Immune Evasion in Lung Adenocarcinoma
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When tiny plastic particles from PET (a common plastic in bottles and clothing) get inhaled, they pick up proteins from lung fluid that essentially disguise them—and in mice with lung cancer, this disguise helped tumors grow faster by tricking the immune system into "cleaning up" cancer cells in a way that actually protects the tumor instead of fighting it. This matters because it suggests breathing in airborne microplastics could make existing lung cancer worse by hijacking the body's normal immune defenses, giving scientists a new potential target for treatment and another reason to take plastic pollution seriously as a health risk
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