ArticleToxicological sciences : an official journal of the Society of Toxicology2011
Reversal and prevention of arsenic-induced human bronchial epithelial cell malignant transformation by microRNA-200b.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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64 citing papers in PubMed, 134 citations in OpenAlex.
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- Tiam1 up-regulation by long non-coding RNA ABHD11-AS1 sponging of miR-182-5p causes β-catenin pathway activation to promote hexavalent chromium lung carcinogenesis.Journal of hazardous materials · 2026Article
- A dynamic model of inorganic arsenic-induced carcinogenesis reveals an epigenetic mechanism for epithelial-mesenchymal plasticity.Environmental pollution (Barking, Essex : 1987) · 2024Article
- Epigenetic downregulation of OEnvironmental pollution (Barking, Essex : 1987) · 2024Article
- Up-regulation of RNA mToxicology and applied pharmacology · 2023Article
- The interaction between miRNAs and hazardous materials.Non-coding RNA research · 2023Review
- Arsenic causing gallbladder cancer disease in Bihar.Scientific reports · 2023Article
- miRNAs and arsenic-induced carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Review
- Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023Article
- MicroRNA-Gene Interactions Impacted by Toxic Metal(oid)s during EMT and Carcinogenesis.Cancers · 2022Review
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- Toxic metals in the regulation of epithelial-mesenchymal plasticity: demons or angels?Cancer cell international · 2022Review
- The Potential Key Role of the NRF2/NQO1 Pathway in the Health Effects of Arsenic Pollution on SCC.International journal of environmental research and public health · 2022Article
- EZH2 inhibition confers PIK3CA-driven lung tumors enhanced sensitivity to PI3K inhibition.Cancer letters · 2022Article
- Down-regulation of lncRNA MEG3 promotes chronic low dose cadmium exposure-induced cell transformation and cancer stem cell-like property.Toxicology and applied pharmacology · 2021Article
- Mechanisms of the synergistic lung tumorigenic effect of arsenic and benzo(a)pyrene combined- exposure.Seminars in cancer biology · 2021Review
- Dysregulation of microRNAs in metal-induced angiogenesis and carcinogenesis.Seminars in cancer biology · 2021Review
- LncRNA DUXAP10 Upregulation and the Hedgehog Pathway Activation Are Critically Involved in Chronic Cadmium Exposure-Induced Cancer Stem Cell-Like Property.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Crosstalk between Environmental Inflammatory Stimuli and Non-Coding RNA in Cancer Occurrence and Development.Cancers · 2021Review
- Paradoxical effects of arsenic in the lungs.Environmental health and preventive medicine · 2021Review
4 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Arsenic is a well-recognized human carcinogen, yet the mechanism by which it causes human cancer has not been elucidated. MicroRNAs (miRNAs) are a big family of small noncoding RNAs and negatively regulate the expression of a large number of protein-coding genes. We investigated the role of miRNAs in arsenic-induced human bronchial epithelial cell malignant transformation and tumor formation. We found that prolonged exposure of immortalized p53-knocked down human bronchial epithelial cells (p53(low)HBECs) to low levels of arsenite (NaAsO₂, 2.5 μM) caused malignant transformation that was accompanied by epithelial to mesenchymal transition (EMT) and reduction in the levels of miR-200 family members. Stably reexpressing miR-200b in arsenite-transformed cells (As-p53(low)HBECs) completely reversed their transformed phenotypes, as evidenced by inhibition of colony formation in soft agar and prevention of xenograft tumor formation in nude mice. Moreover, stably expressing miR-200b alone in parental nontransformed p53(low)HBECs was sufficient to completely prevent arsenite exposure from inducing EMT and malignant transformation. Further mechanistic studies showed that depletion of miR-200 in arsenite-transformed cells involved induction of the EMT-inducing transcription factors zinc-finger E-box-binding homeobox factor 1 (ZEB1) and ZEB2 and increased methylation of miR-200 promoters. Stably expressing ZEB1 alone in parental nontransformed p53(low)HBECs was sufficient to deplete miR-200, induce EMT and cause cell transformation, phenocopying the oncogenic effect of 16-week arsenite exposure. These findings establish for the first time a causal role for depletion of miR-200b expression in human cell malignant transformation and tumor formation resulting from arsenic exposure.
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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.