ArticleToxicological sciences : an official journal of the Society of Toxicology2012
Overabundance of putative cancer stem cells in human skin keratinocyte cells malignantly transformed by arsenic.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- Chronic arsenic exposure induces malignant transformation of human HaCaT cells through both deterministic and stochastic changes in transcriptome expression.Toxicology and applied pharmacology · 2024Article
- Arsenic-induced prostate cancer: an enigma.Medical oncology (Northwood, London, England) · 2024Review
- Article
- Melatonin: a pleiotropic hormone as a novel potent therapeutic candidate in arsenic toxicity.Molecular biology reports · 2021Review
- Environmental chemicals, breast cancer progression and drug resistance.Environmental health : a global access science source · 2020Review
- Polyamine-stimulation of arsenic-transformed keratinocytes.Carcinogenesis · 2019Article
- 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
- 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
- Long-Term Health Effects and Underlying Biological Mechanisms of Developmental Exposure to Arsenic.Current environmental health reports · 2018Review
- NRF2 Is a Potential Modulator of Hyperresistance to Arsenic Toxicity in Stem-Like Keratinocytes.Oxidative medicine and cellular longevity · 2017Article
- Acquisition cancer stemness, mesenchymal transdifferentiation, and chemoresistance properties by chronic exposure of oral epithelial cells to arecoline.Oncotarget · 2016Article
- Mitigation of arsenic-induced acquired cancer phenotype in prostate cancer stem cells by miR-143 restoration.Toxicology and applied pharmacology · 2016Article
- Developmental Windows of Susceptibility to Inorganic Arsenic: A Survey of Current Toxicologic and Epidemiologic Data.Toxicology research · 2016Article
- Cancer Stem-Like Cells Accumulated in Nickel-Induced Malignant Transformation.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Involvement of epigenetics and EMT-related miRNA in arsenic-induced neoplastic transformation and their potential clinical use.Cancer prevention research (Philadelphia, Pa.) · 2015Article
- Arsenical keratosis caused by medication: a case report and literature.International journal of clinical and experimental medicine · 2015Article
- The Use of Chemical-Chemical Interaction and Chemical Structure to Identify New Candidate Chemicals Related to Lung Cancer.PloS one · 2015Article
- Aberrant microRNA expression likely controls RAS oncogene activation during malignant transformation of human prostate epithelial and stem cells by arsenic.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- Actions of endocrine-disrupting chemicals on stem/progenitor cells during development and disease.Endocrine-related cancer · 2014Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Arsenic is a human skin carcinogen. Cancer is probably a disease driven by stem cells (SCs), and SCs are likely a key target during arsenic oncogenesis. In utero arsenic exposure predisposes mice to skin cancers that overproduce cancer SCs (CSCs) and have distorted CSC signaling and population dynamics. Therefore, we hypothesized CSC accumulation may occur during arsenic-induced malignant transformation in vitro of human skin keratinocytes. Thus, the HaCaT cell line, malignantly transformed by arsenite (100 nM, 30 weeks; termed As-TM cells) in prior work, was further studied for the quantity and nature of SCs after this transformation. SCs were isolated from passage-matched control and As-TM cells by a magnetic bead system that enriches for CD34-positive cells. There were 2.5 times more SCs isolated from As-TM cells than control. Holoclone production from As-TM putative CSCs was 2.5-fold higher by 1 week and 3.5-fold higher by 2 weeks than control SCs. Potential malignant phenotype was assessed in isolated SC/CSCs. Transcript level of SC/CSC markers were elevated in both isolated As-TM CSCs and control SCs compared with parental cells, but compared with control SCs, As-TM putative CSCs had elevated CD34, K5, K14, K15, and K19 transcripts and dramatically stronger staining for p63, Rac1, K5, Notch1, and K19. As-TM putative CSCs also showed markedly elevated MMP-9 secretion and colony formation, indicators of cancer phenotype, even compared with total population of As-TM cells. Thus, malignant phenotype is particularly pronounced in CSCs after arsenic-induced transformation of human skin cells and occurs concurrently with a potential overproduction of these cells.
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