ArticleOncotarget2014
Arsenic-induced sub-lethal stress reprograms human bronchial epithelial cells to CD61¯ cancer stem cells.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Aryl Hydrocarbon Receptor (AHR) Suppresses Arsenic (AsInternational journal of biological sciences · 2025Article
- Arsenic Activates the ER Stress-Associated Unfolded Protein Response via the Activating Transcription Factor 6 in Human Bronchial Epithelial Cells.Biomedicines · 2022Article
- Oxidative Stress and Cancer Heterogeneity Orchestrate NRF2 Roles Relevant for Therapy Response.Molecules (Basel, Switzerland) · 2022Review
- Arsenic activates STAT3 signaling during the transformation of the human bronchial epithelial cells.Toxicology and applied pharmacology · 2022Article
- Metabolomic dynamics of the arsenic-transformed bronchial epithelial cells and the derived cancer stem-like cells.International journal of biological sciences · 2022Article
- Cooperation between NRF2-mediated transcription and MDIG-dependent epigenetic modifications in arsenic-induced carcinogenesis and cancer stem cells.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
- Connections between endoplasmic reticulum stress-associated unfolded protein response, mitochondria, and autophagy in arsenic-induced carcinogenesis.Seminars in cancer biology · 2021Review
- Long-term arsenic exposure impairs differentiation in mouse embryonal stem cells.Journal of applied toxicology : JAT · 2021Article
- Environmentally-inducedTheranostics · 2021Article
- Nrf2 and HIF1α converge to arsenic-induced metabolic reprogramming and the formation of the cancer stem-like cells.Theranostics · 2020Article
- Environmental exposures, stem cells, and cancer.Pharmacology & therapeutics · 2019Review
- Metabolic and epigenetic reprogramming in the arsenic-induced cancer stem cells.Seminars in cancer biology · 2019Review
- Metal carcinogen exposure induces cancer stem cell-like property through epigenetic reprograming: A novel mechanism of metal carcinogenesis.Seminars in cancer biology · 2019Review
- A review of arsenic exposure and lung cancer.Toxicology research · 2019Review
- Arsenic promotes the COX2/PGE2-SOX2 axis to increase the malignant stemness properties of urothelial cells.International journal of cancer · 2018Article
- Long-Term Health Effects and Underlying Biological Mechanisms of Developmental Exposure to Arsenic.Current environmental health reports · 2018Review
- Cancer Stem Cells: Emergent Nature of Tumor Emergency.Frontiers in genetics · 2018Article
- The role of cancer-associated fibroblast MRC-5 in pancreatic cancer.Journal of Cancer · 2018Article
- Inactivation of miR-100 combined with arsenic treatment enhances the malignant transformation of BEAS-2B cells via stimulating epithelial -mesenchymal transition.Cancer biology & therapy · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
In the present report, we demonstrate that sub-lethal stress induced by consecutive exposure to 0.25 µM arsenic (As3+) for six months can trigger reprogramming of the human bronchial epithelial cell (BEAS-2B) to form cancer stem cells (CSCs) without forced introduction of the stemness transcription factors. These CSCs formed from As3+-induced sub-lethal stress featured with an increased expression of the endogenous stemness genes, including Oct4, Sox2, Klf4, Myc, and others that are associated with the pluripotency and self-renewal of the CSCs. Flow cytometry analysis indicated that 90% of the CSC cells are CD61¯, whereas 100% of the parental cells are CD61+. These CD61¯ CSCs are highly tumorigenic and metastatic to the lung in xenotransplantation tests in NOD/SCID Il2rγ-/- mice. Additional tests also revealed that the CD61¯ CSCs showed a significant decrease in the expression of the genes important for DNA repair and oxidative phosphorylation. To determine the clinical relevance of the above findings, we stratified human lung cancers based on the level of CD61 protein and found that CD61low cancer correlates with poorer survival of the patients. Such a correlation was also observed in human breast cancer and ovarian cancer. Taken together, our findings suggest that in addition to the traditional approaches of enforced introduction of the exogenous stemness circuit transcription factors, sub-lethal stress induced by consecutive low dose As3+ is also able to convert non-stem cells to the CSCs.
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