ArticleToxicological sciences : an official journal of the Society of Toxicology2022
Chronic Hexavalent Chromium Exposure Upregulates the RNA Methyltransferase METTL3 Expression to Promote Cell Transformation, Cancer Stem Cell-Like Property, and Tumorigenesis.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- AB-Free Kava and Dihydromethysticin Inhibit Chronic Hexavalent Chromium Exposure-Induced Cell Malignant Transformation through Down-Regulating RNA Splicing Factor SNRPA1 Expression.Chemical research in toxicology · 2026Article
- 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
- Associations of children's urinary metals with blood RNA NEnvironmental research · 2025Article
- Epitranscriptomic sculpting: the role of mMedical oncology (Northwood, London, England) · 2025Review
- The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024Review
- Dysregulation of Long Non-coding RNAs-the Novel lnc in Metal Toxicity and Carcinogenesis.Current environmental health reports · 2024Review
- Carcinogenic Mechanisms of Hexavalent Chromium: From DNA Breaks to Chromosome Instability and Neoplastic Transformation.Current environmental health reports · 2024Review
- Acute particulate hexavalent chromium exposure induces DNA double-strand breaks and activates homologous recombination repair in rat lung tissue.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Long noncoding RNA ABHD11-AS1 interacts with SART3 and regulates CD44 RNA alternative splicing to promote lung carcinogenesis.Environment international · 2024Article
- Epigenetic downregulation of OEnvironmental pollution (Barking, Essex : 1987) · 2024Article
- Up-regulation of RNA mToxicology and applied pharmacology · 2023Article
- New insights into the regulation of METTL3 and its role in tumors.Cell communication and signaling : CCS · 2023Review
- Effects of Gestational Arsenic Exposures on Placental and Fetal Development in Mice: The Role ofEnvironmental health perspectives · 2023Article
- Molecular mechanisms of environmental exposures and human disease.Nature reviews. Genetics · 2023Review
- Epigenetic and epitranscriptomic mechanisms of chromium carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Article
- The Epitranscriptomic Mechanism of Metal Toxicity and Carcinogenesis.International journal of molecular sciences · 2022Review
- Cancer-Associated Fibroblasts Hinder Lung Squamous Cell Carcinoma Oxidative Stress-Induced Apoptosis via METTL3 Mediated mOxidative medicine and cellular longevity · 2022Article
- Regulatory Network of Methyltransferase-Like 3 in Stem Cells: Mechanisms and Medical Implications.Cell transplantationReview
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Hexavalent chromium [Cr(VI)] is a common environmental carcinogen causing lung cancer in humans. This study investigates the mechanism of Cr(VI) carcinogenesis focusing on the role of the epitranscriptomic dysregulation. The epitranscriptomic effect of Cr(VI) was determined in Cr(VI)-transformed human bronchial epithelial cells, chromate-exposed mouse and human lungs. The epitranscriptomic effect and its role in Cr(VI)-induced cell transformation, cancer stem cell (CSC)-like property, and tumorigenesis were determined by microarray analysis, soft agar colony formation, suspension spheroid formation, and mouse xenograft tumorigenesis assays. It was found that chronic Cr(VI) exposure causes epitranscriptomic dysregulations as evidenced by the increased levels of total RNA N6-methyladenosine (m6A) modification and the RNA m6A methyltransferase like-3 (METTL3) in Cr(VI)-transformed cells and chromate exposure-caused mouse and human lung tumors. Knockdown of METTL3 expression in Cr(VI)-transformed cells significantly reduces their m6A levels and transformed phenotypes and tumorigenicity in mice. Moreover, knockdown of METTL3 expression in parental nontransformed cells significantly reduces the capability of chronic Cr(VI) exposure to induce cell transformation and CSC-like property. Together, this study reveals that chronic Cr(VI) exposure is capable of altering cellular epitranscriptome by increasing the m6A RNA modification via upregulating the RNA methyltransferase METTL3 expression, which plays an important role in Cr(VI)-induced cell transformation, CSC-like property, and tumorigenesis.
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