ArticleToxicology and applied pharmacology2016
Mitigation of arsenic-induced acquired cancer phenotype in prostate cancer stem cells by miR-143 restoration.
Article in Toxicology and applied pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed, 44 citations in OpenAlex.
- Urinary Trace Element Concentrations in Congolese Patients With Prostate Cancer: A Case-Control Study.Prostate cancer · 2026Article
- Toxicology of Airborne Inorganic Arsenic: Oxidative Stress, Molecular Mechanisms, and Organ-Specific Pathologies.Toxics · 2025Review
- The Role of RAC2 and PTTG1 in Cancer Biology.Cells · 2025Review
- A Critical Review on microRNAs as Prognostic Biomarkers in Laryngeal Carcinoma.International journal of molecular sciences · 2024Review
- Prostate Cancer: Emerging Modifiable Risk Factors and Therapeutic Strategies in the Management of Advanced Cancer.Life (Basel, Switzerland) · 2024Review
- Arsenic toxicity: sources, pathophysiology and mechanism.Toxicology research · 2024Review
- Arsenic-induced prostate cancer: an enigma.Medical oncology (Northwood, London, England) · 2024Review
- Role of actin-binding proteins in prostate cancer.Frontiers in cell and developmental biology · 2024Review
- Review
- Targeting of AKT1 by miR-143-3p Suppresses Epithelial-to-Mesenchymal Transition in Prostate Cancer.Cells · 2023Article
- miRNAs and arsenic-induced carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Review
- Arsenic activates STAT3 signaling during the transformation of the human bronchial epithelial cells.Toxicology and applied pharmacology · 2022Article
- The role of autophagy in metal-induced urogenital carcinogenesis.Seminars in cancer biology · 2021Review
- Dysregulation of microRNAs in metal-induced angiogenesis and carcinogenesis.Seminars in cancer biology · 2021Review
- Health Effects Associated With Pre- and Perinatal Exposure to Arsenic.Frontiers in genetics · 2021Review
- Metals and molecular carcinogenesis.Carcinogenesis · 2020Review
- Environmental exposures, stem cells, and cancer.Pharmacology & therapeutics · 2019Review
- Review
- Metal carcinogen exposure induces cancer stem cell-like property through epigenetic reprograming: A novel mechanism of metal carcinogenesis.Seminars in cancer biology · 2019Review
- Arsenic Alters Exosome Quantity and Cargo to Mediate Stem Cell Recruitment Into a Cancer Stem Cell-Like Phenotype.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Inorganic arsenic, an environmental contaminant and a human carcinogen is associated with prostate cancer. Emerging evidence suggests that cancer stem cells (CSCs) are the driving force of carcinogenesis. Chronic arsenic exposure malignantly transforms the human normal prostate stem/progenitor cell (SC) line, WPE-stem to arsenic-cancer SCs (As-CSCs), through unknown mechanisms. MicroRNAs (miRNAs) are small, non-coding RNAs that negatively regulate gene expression at the posttranscriptional level. In prior work, miR-143 was markedly downregulated in As-CSCs, suggesting a role in arsenic-induced malignant transformation. In the present study, we investigated whether loss of miR-143 expression is important in arsenic-induced transformation of prostate SCs. Restoration of miR-143 in As-CSCs was achieved by lentivirus-mediated miR-143 overexpression. Cells were assessed bi-weekly for up to 30weeks to examine mitigation of cancer phenotype. Secreted matrix metalloproteinase (MMP) activity was increased by arsenic-induced malignant transformation, but miR-143 restoration decreased secreted MMP-2 and MMP-9 enzyme activities compared with scramble controls. Increased cell proliferation and apoptotic resistance, two hallmarks of cancer, were decreased upon miR-143 restoration. Increased apoptosis was associated with decreased BCL2 and BCL-XL expression. miR-143 restoration dysregulated the expression of SC/CSC self-renewal genes including NOTCH-1, BMI-1, OCT4 and ABCG2. The anticancer effects of miR-143 overexpression appeared to be mediated by targeting and inhibiting LIMK1 protein, and the phosphorylation of cofilin, a LIMK1 substrate. These findings clearly show that miR-143 restoration mitigated multiple cancer characteristics in the As-CSCs, suggesting a potential role in arsenic-induced transformation of prostate SCs. Thus, miR-143 is a potential biomarker and therapeutic target for arsenic-induced prostate cancer.
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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.