ArticleToxicological sciences : an official journal of the Society of Toxicology2019
Chronic Hexavalent Chromium Exposure Induces Cancer Stem Cell-Like Property and Tumorigenesis by Increasing c-Myc Expression.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2019. 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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Who cites it
27 citing papers in PubMed, 45 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
- METTL3 in Cr (VI)-induced carcinogenesis and CXCL6 expression associated with lung cancer development.Genes & diseases · 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
- Dysregulation of Long Non-coding RNAs-the Novel lnc in Metal Toxicity and Carcinogenesis.Current environmental health reports · 2024Review
- Stress granules play a critical role in hexavalent chromium-induced malignancy in a G3BP1 dependent manner.Environmental pollution (Barking, Essex : 1987) · 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
- The interaction between miRNAs and hazardous materials.Non-coding RNA research · 2023Review
- Article
- Epigenetic and epitranscriptomic mechanisms of chromium carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Chromium (VI)-induced ALDH1A1/EGF axis promotes lung cancer progression.Clinical and translational medicine · 2022Article
- Review
- Loss of MEG3 and upregulation of miR-145 play an important role in the invasion and migration of Cr(VI)-transformed cells.Heliyon · 2022Article
- Chronic Hexavalent Chromium Exposure Upregulates the RNA Methyltransferase METTL3 Expression to Promote Cell Transformation, Cancer Stem Cell-Like Property, and Tumorigenesis.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Epigenetic Regulation in Exposome-Induced Tumorigenesis: Emerging Roles of ncRNAs.Biomolecules · 2022Review
- Particulate hexavalent chromium alters microRNAs in human lung cells that target key carcinogenic pathways.Toxicology and applied pharmacology · 2022Article
- Dysregulation of microRNAs in metal-induced angiogenesis and carcinogenesis.Seminars in cancer biology · 2021Review
- Mechanisms of the synergistic lung tumorigenic effect of arsenic and benzo(a)pyrene combined- exposure.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
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Hexavalent chromium [Cr(VI)] is one of the most common environmental carcinogen causing lung cancer in humans; however, the mechanism of Cr(VI) carcinogenesis remains elusive. Cancer stem cells (CSCs) are considered as cancer initiating and maintaining cells. Ours and other recent studies showed that chronic Cr(VI) exposure induces CSC-like property representing an important mechanism of Cr(VI) carcinogenesis. However, how Cr(VI) exposure induces CSC-like property remains largely unknown. In this study, we found that stably knocking down the expression of c-Myc, a proto-oncogene and one of key stemness factors playing critical roles in cancer initiation and progression, in Cr(VI)-transformed human bronchial epithelial cells [BEAS-2B-Cr(VI)] significantly decreased their CSC-like property and tumorigenicity in mice. Moreover, stably knocking down c-Myc expression in parental nontransformed BEAS-2B cells significantly impaired the capability of chronic Cr(VI) exposure to induce CSC-like property and cell transformation. It was also found that stably overexpressing c-Myc alone in parental nontransformed BEAS-2B cells is capable of causing CSC-like property and cell transformation. Mechanistic studies showed that chronic Cr(VI) exposure increases c-Myc expression by down-regulating the level of microRNA-494 (miR-494). It was further determined that overexpressing miR-494 significantly reduces Cr(VI)-induced CSC-like property, cell transformation, and tumorigenesis mainly through down-regulating c-Myc expression. Together, these findings indicate that chronic low dose Cr(VI) exposure induces CSC-like property and tumorigenesis by increasing c-Myc expression through down-regulating the level of miR-494, revealing an important role of the proto-oncogene c-Myc in Cr(VI) carcinogenesis.
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