ArticleToxicological sciences : an official journal of the Society of Toxicology2018
Arsenic Alters Exosome Quantity and Cargo to Mediate Stem Cell Recruitment Into a Cancer Stem Cell-Like Phenotype.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- Small extracellular vesicles are the key players in ochratoxin A-induced kidney toxicity.Cell communication and signaling : CCS · 2026Article
- Extracellular Vesicles and Endocrine Disruption: How Environmental Pollutants Modulate the Loading and Release of Extracellular Vesicles for Cancer Promotion and Progression.International journal of molecular sciences · 2026Review
- Rethinking the microenvironment's role in chemical-induced malignancy.Toxicological sciences : an official journal of the Society of Toxicology · 2026Review
- Urinary Trace Element Concentrations in Congolese Patients With Prostate Cancer: A Case-Control Study.Prostate cancer · 2026Article
- Extracellular Vesicle (EV) Mechanisms of Toxicity for Per and Polyfluoroalkyl Substances: Comparing Transcriptomic Points of Departure Across Global Versus EV Regulatory Gene Sets.Environmental and molecular mutagenesis · 2025Article
- Characterization of extracellular vesicles and miRNA released by cerebral organoids.Current research in toxicology · 2025Article
- Arsenic-induced prostate cancer: an enigma.Medical oncology (Northwood, London, England) · 2024Review
- Exposome and unhealthy aging: environmental drivers from air pollution to occupational exposures.GeroScience · 2023Review
- Arsenic and Human Health: New Molecular Mechanisms For Arsenic-Induced Cancers.Current pollution reports · 2023Article
- Periconceptional and Prenatal Exposure to Metals and Extracellular Vesicle and Particle miRNAs in Human Milk: A Pilot Study.Exposure and health · 2023Article
- Arsenic disrupts extracellular vesicle-mediated signaling in regenerating myofibers.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Molecular mechanisms of environmental exposures and human disease.Nature reviews. Genetics · 2023Review
- The impact of environmental contaminants on extracellular vesicles and their key molecular regulators: A literature and database-driven review.Environmental and molecular mutagenesis · 2023Review
- miRNAs and arsenic-induced carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Review
- Urinary metals and maternal circulating extracellular vesicle microRNA in the MADRES pregnancy cohort.Epigenetics · 2022Article
- Environmental Exposures and Extracellular Vesicles: Indicators of Systemic Effects and Human Disease.Current environmental health reports · 2022Review
- Current Advances of Nanomedicines Delivering Arsenic Trioxide for Enhanced Tumor Therapy.Pharmaceutics · 2022Review
- Nanoplastics and Arsenic Co-Exposures Exacerbate Oncogenic Biomarkers under an In Vitro Long-Term Exposure Scenario.International journal of molecular sciences · 2022Article
- Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications.International journal of molecular sciences · 2021Review
- Underlying metastasis mechanism and clinical application of exosomal circular RNA in tumors (Review).International journal of oncology · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Inorganic arsenic is a human carcinogen that can target the prostate. Accumulating evidence suggests arsenic can disrupt stem cell (SC) dynamics during the carcinogenic process. Previous work demonstrated arsenic-transformed prostate epithelial (CAsE-PE) cells can recruit prostate SCs into rapidly acquiring a cancer SC (CSC) phenotype via the secretion of soluble factors. Exosomes are small, membrane-derived vesicles that contain lipids, RNA, and proteins, and actively contribute to cancer initiation and progression when taken up by target cells. Here we hypothesized that CAsE-PE cells are recruiting SCs to a CSC-like phenotype via exosomal signaling. CAsE-PE cells secreted 700% more exosomes than parental RWPE-1 cells. CAsE-PE exosomes were enriched with oncogenic factors, including oncogenes (KRAS, NRAS, VEFGA, MYB, and EGFR), inflammation-related (cyclooxygenase-2, interleukin 1B (IL1B), IL6, transforming growth factor-β, and tumor necrosis factor-A), and apoptosis-related (CASP7, CASP9, and BCL2) transcripts, and oncogenesis-associated microRNAs. When compared with SCs cultured in exosome-depleted conditioned medium (CM), SCs cultured in CM containing CAsE-PE-derived exosomes showed increased (198%) matrix metalloproteinase activity and underwent an epithelial-to-mesenchymal transition in morphology, suggesting an exosome-mediated transformation. KRAS plays an important role in arsenic carcinogenesis. Although KRAS transcript (>24 000%) and protein (866%) levels were elevated in CAsE-PE exosomes, knock-down of KRAS in these cells only partially mitigated the CSC-like phenotype in cocultured SCs. Collectively, these results suggest arsenic impacts both exosomal quantity and cargo. Exosomal KRAS is only minimally involved in this recruitment, and additional factors (eg, cancer-associated miRNAs) likely also play a role. This work furthers our mechanistic understanding of how arsenic disrupts SC dynamics and influences the tumor microenvironment during carcinogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.