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20 resultsShowing papers similar to Polystyrene Nanoplasticsat an Environmentally RelevantConcentration Promote Ovarian Cancer Progression via CDK4/6-DependentSignaling
ClearPolystyrene Nanoplastics at an Environmentally Relevant Concentration Promote Ovarian Cancer Progression via CDK4/6-Dependent Signaling
Researchers demonstrated that polystyrene nanoplastics at concentrations as low as 20 μg/mL—consistent with environmental exposure levels—significantly promoted ovarian cancer cell proliferation through CDK4/6 signaling, providing evidence of a potential carcinogenic risk from nanoplastic exposure.
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.
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.
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.
Polystyrene nanoplastics induce ovarian granulosa cell senescence via autophagy suppression
Researchers found that polystyrene nanoplastics induce premature cellular aging (senescence) in human ovarian granulosa cells by suppressing autophagy, triggering inflammatory signaling and mitochondrial dysfunction, and that restoring autophagy with rapamycin reversed these effects — pointing to a potential mechanism linking nanoplastic exposure to accelerated ovarian aging.
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.
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.
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.
Polystyrene nanoplastics induce ovarian injury by PI3K-Akt pathway-driven macrophage extracellular trap formation
Researchers showed that polystyrene nanoplastics accumulate in mouse ovaries, triggering macrophage infiltration and the formation of macrophage extracellular traps (METs) via the PI3K-Akt signaling pathway, which in turn cause pyroptosis (inflammatory cell death) in granulosa cells and follicular loss — effects reversible with a PI3K inhibitor.
Polystyrene nanoplastics impair endometrial decidualization via cell cycle arrest and JNK-MAPK pathway-mediated oxidative stress in early pregnant mice
Researchers found that polystyrene nanoplastics disrupt uterine lining preparation for embryo implantation in early pregnant mice by blocking cell cycle progression and triggering oxidative stress via the JNK-MAPK signaling pathway, with JNK pathway inhibition partially restoring normal decidualization and improving embryo implantation outcomes.
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.
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.
Polystyrene nanoplastics induce apoptosis, autophagy, and steroidogenesis disruption in granulosa cells to reduce oocyte quality and fertility by inhibiting the PI3K/AKT pathway in female mice
Researchers found that polystyrene nanoplastics (tiny plastic particles under 1 micrometer) impair egg cell quality in female mice by damaging the ovarian support cells that help eggs mature, triggering cell death and disrupting hormone production. These findings raise important questions about the potential reproductive risks of nanoplastic exposure in women.
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.
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.
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.
Carboxylate polystyrene nanoplastics disrupt mitotic progression and induce chromosomal instability
Researchers found that carboxylate polystyrene nanoplastics accumulated near centrosomes in cells and induced supernumerary centrioles, leading to abnormal spindle formation and chromosomal instability during cell division, revealing a mechanism by which nanoplastics may cause heritable genetic damage.
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.
Comparative evaluation of molecular mechanisms triggered by differently functionalized polystyrene nanoplastics in human colon cell lines
Researchers compared the molecular responses triggered by polystyrene nanoplastics with different surface chemical groups in human colon cell lines. The study investigated how the specific functionalization of nanoplastic surfaces influences the cellular and molecular pathways activated upon exposure in human intestinal tissue.