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20 resultsShowing papers similar to Polystyrene Nanoplastics at an Environmentally Relevant Concentration Promote Ovarian Cancer Progression via CDK4/6-Dependent Signaling
ClearPolystyrene Nanoplasticsat an Environmentally RelevantConcentration Promote Ovarian Cancer Progression via CDK4/6-DependentSignaling
Researchers found that polystyrene nanoplastics at environmentally relevant concentrations (20 μg/mL) promoted ovarian cancer cell proliferation through CDK4/6-dependent signaling, representing the first evidence that environmentally relevant nanoplastic levels may drive ovarian cancer progression.
Polystyrene nanoparticle exposure accelerates ovarian cancer development in mice by altering the tumor microenvironment
A study in mice found that exposure to tiny polystyrene nanoplastics (100 nanometers) through drinking water significantly accelerated the growth of ovarian cancer tumors. The nanoplastics altered the tumor's surrounding environment and disrupted immune-related gene expression, creating conditions that favored cancer progression. This is concerning because it suggests everyday nanoplastic exposure could potentially worsen cancer outcomes in humans.
Long-term exposure to nanoplastics alters molecular and functional traits related to the carcinogenic process
Researchers exposed cells to polystyrene nanoplastics for six months and found that long-term exposure activated multiple molecular markers associated with cancer development, including enhanced cell migration, invasion potential, and ability to grow independently. The study suggests that chronic nanoplastic exposure may pose a carcinogenic risk, though further research is needed to confirm these findings in living organisms.
Effect of Polystyrene Nanoplastics on Ovarian Granulosa Cells
Researchers exposed human granulosa-like tumor cells to polystyrene nanoplastics at increasing concentrations and measured cell viability, membrane damage, and apoptosis. Nanoplastic exposure reduced cell viability in a dose-dependent manner with an IC50 indicating significant cytotoxicity, suggesting potential harm to female ovarian granulosa cells from nanoplastic exposure.
Assessment of cancer-related signaling pathways in responses to polystyrene nanoplastics via a kidney-testis microfluidic platform (KTP)
Researchers developed a kidney-testis microfluidic platform to assess cancer-related signaling pathway responses to polystyrene nanoplastics. The study found that nanoplastic exposure activated cancer-associated signaling pathways in both kidney and testis tissue models, providing new insights into the potential molecular mechanisms through which nanoplastics may affect organ health.
Insights into the potential carcinogenicity of micro- and nano-plastics.
This review examined existing evidence on the carcinogenic potential of micro- and nano-plastics, finding studies demonstrating genotoxicity, oxidative DNA damage, disruption of cell signaling, and tumor-promoting effects, while noting that direct human carcinogenicity data remain limited and mechanistic pathways require further investigation.
Micro(nano)plastics pollution and human health: How plastics can induce carcinogenesis to humans?
This review examines how microplastics and nanoplastics enter the human body through food, water, and air, and how they may contribute to cancer development. Common plastic types like polystyrene and PVC, along with toxic chemicals they carry such as PAHs and PCBs, have been linked to DNA damage, oxidative stress, and inflammation, all of which can promote cancer. The paper highlights that while the evidence is growing, more research is needed to understand the full cancer risk from chronic microplastic exposure.
Microplastics as emerging carcinogens: from environmental pollutants to oncogenic drivers
This review examines growing evidence that microplastics and nanoplastics may play a role in cancer development, with these particles found in human tumor tissues from the lungs, colon, stomach, breast, and other organs. The particles appear to promote cancer through chronic inflammation, oxidative stress, DNA damage, and disruption of key cancer-related signaling pathways. While direct proof of causation in humans is still lacking, the accumulating evidence from lab studies, animal experiments, and human tissue analysis suggests microplastics deserve serious attention as potential contributors to cancer risk.
Nanoplastics as a Potential Environmental Health Factor: From Molecular Interaction to Altered Cellular Function and Human Diseases
This review examined how nanoplastics — particularly polystyrene — interact with cells at the molecular level, potentially causing lasting changes that could contribute to developmental problems and degenerative disease. The study highlights growing concerns about nanoplastics as an emerging environmental health risk given their widespread presence in food, water, and air.
Long-term low-dose exposure to polystyrene nanoplastics induces morphological and transcriptional reprogramming to enhance metastatic potential of colorectal cancer cells
Researchers exposed colorectal cancer cells to low doses of 20-nanometer polystyrene nanoplastics over an extended period and found that the cells underwent significant morphological and genetic changes that enhanced their ability to migrate and metastasize. The nanoplastic-treated cells showed increased markers for cancer stem cell properties and epithelial-mesenchymal transition. Zebrafish models confirmed that nanoplastic exposure accelerated the spread of colorectal cancer cells, suggesting nanoplastics may contribute to cancer progression.
Exposure to polystyrene nanoparticles leads to dysfunction in DNA repair mechanisms in Caco-2 cells
Researchers found that exposing intestinal cells (Caco-2) to polystyrene nanoplastics impaired DNA repair mechanisms even at doses that didn't kill the cells, raising concern that nanoplastic exposure could lead to genetic instability and long-term health risks over time.
Effects of polystyrene nanoplastics on the female reproductive system in mice: Implications for ovarian function and follicular development
Researchers exposed female mice to polystyrene nanoplastics orally for 29 days and examined the effects on their reproductive systems. They found that nanoplastic exposure disrupted estrous cycles, impaired follicle development, and altered hormone levels in a dose-dependent manner. The study suggests that nanoplastics, due to their extremely small size, may cross biological barriers and accumulate in reproductive tissues, raising concerns about potential effects on fertility.
Polystyrene nanoplastics exposure caused defective neural tube morphogenesis through caveolae-mediated endocytosis and faulty apoptosis
This study found that polystyrene nanoplastics caused abnormal neural tube formation in early embryonic development by being taken up through a specific cellular pathway and triggering defective cell death. The findings suggest nanoplastics could potentially interfere with fetal brain development, raising serious concerns about exposure during pregnancy.
Evaluating the relationship between microplastics and nanoplastics contamination and diverse cancer types development
This review examines growing evidence that micro- and nanoplastics found in human tissues may contribute to cancer development through several pathways. These tiny particles can generate harmful molecules called reactive oxygen species, cause chronic inflammation, and disrupt cell growth signals, all of which are known to promote cancer. While long-term, high-level exposure likely poses the greatest risk, more research is needed to understand the full cancer-related dangers of microplastic exposure.
Micro and nanoplastics in human carcinogenesis: Insights from in vitro studies
This narrative review compiles in vitro evidence on the carcinogenic effects of micro- and nanoplastics across multiple cancer types, examining mechanisms including oxidative stress, DNA damage, immune dysregulation, and epigenetic changes identified in cell culture experiments.
The ovarian-related effects of polystyrene nanoplastics on human ovarian granulosa cells and female mice
This study tested the effects of polystyrene nanoplastics on both human ovarian cells in the lab and on female mice. The nanoplastics accumulated in ovarian tissue, caused cell death, disrupted hormone levels, and reduced egg quality and fertility in mice. These findings suggest that nanoplastic exposure could threaten female reproductive health by damaging the ovaries.
Exposure to polystyrene nanoplastics induces lysosomal enlargement and lipid droplet accumulation in KGN human ovarian granulosa cells
Researchers exposed human ovarian cells to polystyrene nanoplastics and found that the particles entered the cells and caused abnormal enlargement of lysosomes (cellular recycling structures) and accumulation of fat droplets. These changes occurred even at concentrations that did not kill the cells outright, suggesting subtle but potentially significant damage. The findings point to a possible mechanism by which nanoplastics could impair female reproductive health.
Cytotoxicity and pro-inflammatory effect of polystyrene nano-plastic and micro-plastic on RAW264.7 cells.
Researchers found that polystyrene nano-plastics (80 nm) induced apoptosis and pro-inflammatory cytokine release in mouse macrophage RAW264.7 cells at lower concentrations than micro-plastics (3 μm), with nano-plastics also enhancing phagocytic activity and activating NF-kB signaling pathways more potently than their larger counterparts.
Polystyrene nanoplastics mediate oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line
A cell study found that polystyrene nanoplastics cause dose-dependent damage to human lung cells, triggering oxidative stress, premature cell aging, and cell death. These findings suggest that breathing in nanoplastics could harm lung tissue over time and potentially contribute to cancer risk from air pollution.
Polystyrene nanoplastics disrupt ovarian development via cytoskeletal remodeling and epigenetic reprogramming particularly in granulosa cells
Researchers used single-cell RNA sequencing to map polystyrene nanoplastic toxicity in mouse ovaries, identifying granulosa cells as the primary target and showing that 100 nm particles trigger F-actin cytoskeletal remodeling, STAT1-driven epigenetic reprogramming, and necroptosis, disrupting follicle development and hormone production.