ArticleMolecular carcinogenesis2018
Role of miR-31 and SATB2 in arsenic-induced malignant BEAS-2B cell transformation.
Article in Molecular carcinogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- SATB2 dysregulation generates a novel circular RNA and drives KRAS-like transcriptional reprogramming and transformation-associated phenotypes.Cell communication and signaling : CCS · 2026Article
- Arsenic promotes ROS-mediated malignant transformation of bronchial epithelial cells by specifically downregulating TXNL1 expression.Communications biology · 2025Article
- Toxicology of Airborne Inorganic Arsenic: Oxidative Stress, Molecular Mechanisms, and Organ-Specific Pathologies.Toxics · 2025Review
- Exposure-associated DNA methylation among people exposed to multiple industrial pollutants.Clinical epigenetics · 2024Article
- A dynamic model of inorganic arsenic-induced carcinogenesis reveals an epigenetic mechanism for epithelial-mesenchymal plasticity.Environmental pollution (Barking, Essex : 1987) · 2024Article
- Arsenic toxicity: sources, pathophysiology and mechanism.Toxicology research · 2024Review
- The interaction between miRNAs and hazardous materials.Non-coding RNA research · 2023Review
- miRNAs and arsenic-induced carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Review
- Review
- Article
- p62 functions as a signal hub in metal carcinogenesis.Seminars in cancer biology · 2021Review
- Paradoxical effects of arsenic in the lungs.Environmental health and preventive medicine · 2021Review
- ATF3 Promotes Arsenic-Induced Apoptosis and Oppositely Regulates DR5 and Bcl-xL Expression in Human Bronchial Epithelial Cells.International journal of molecular sciences · 2021Article
- Wrong place, wrong time: Runt-related transcription factor 2/SATB2 pathway in bone development and carcinogenesis.Journal of carcinogenesis · 2021Review
- Role of non-coding-RNAs in response to environmental stressors and consequences on human health.Redox biology · 2020Review
- ICAM5 as a Novel Target for Treating Cognitive Impairment in Fragile X Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Deregulation of SATB2 in carcinogenesis with emphasis on miRNA-mediated control.Carcinogenesis · 2019Review
- MicroRNAs and their role in environmental chemical carcinogenesis.Environmental geochemistry and health · 2019Review
- MicroRNA-874 functions as a tumor suppressor in rhabdomyosarcoma by directly targeting GEFT.American journal of cancer research · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Arsenic is a naturally occurring and highly potent metalloid known to elicit serious public health concerns. Today, approximately 200 million people around the globe are exposed to arsenic-contaminated drinking water at levels greater than the World Health Organization's recommended limit of 10 parts per billion. As a class I human carcinogen, arsenic exposure is known to elicit various cancers, including lung, skin, liver, and kidney. Current evidence suggests that arsenic is capable of inducing both genotoxic and cytotoxic injury, as well as activating epigenetic pathways to induce carcinogenesis. Our study identifies a novel pathway that is implicated in arsenic-induced carcinogenesis. Arsenic down-regulated miRNA-31 and the release of this inhibition caused overexpression of special AT-rich sequence-binding protein 2 (SATB2). Arsenic is known to disrupt miRNA expression, and here we report for the first time that arsenic is capable of inhibiting miR-31 expression. As a direct downstream target of miR-31, SATB2 is a prominent transcription factor, and nuclear matrix binding protein implicated in many types of human diseases including lung cancer. Results from this study show that arsenic induces the overexpressing SATB2 by inhibiting miR-31 expression, which blocks the translation of SATB2 mRNA, since levels of SATB2 mRNA remain the same but protein levels decrease. Overexpression of SATB2 induces malignant transformation of human bronchial epithelial (BEAS-2B) cells indicating the importance of the expression of miR-31 in preventing carcinogenesis by suppressing SATB2 protein levels.
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Registered trials
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.