ArticleToxicology and applied pharmacology2015
Chronic inorganic arsenic exposure in vitro induces a cancer cell phenotype in human peripheral lung epithelial cells.
Article in Toxicology and applied pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- A systematic review and meta-analysis of bidirectional effect of arsenic on ERK signaling pathway.Molecular medicine reports · 2018Pooled it
- A dynamic model of inorganic arsenic-induced carcinogenesis reveals an epigenetic mechanism for epithelial-mesenchymal plasticity.Environmental pollution (Barking, Essex : 1987) · 2024Article
- Arsenic impairs stem cell differentiation via the Hippo signaling pathway.Toxicology research · 2023Article
- Toxic metals in the regulation of epithelial-mesenchymal plasticity: demons or angels?Cancer cell international · 2022Review
- Nanoplastics and Arsenic Co-Exposures Exacerbate Oncogenic Biomarkers under an In Vitro Long-Term Exposure Scenario.International journal of molecular sciences · 2022Article
- Genome-wide expression screening in the cardiac embryonic stem cell test shows additional differentiation routes that are regulated by morpholines and piperidines.Current research in toxicology · 2022Article
- Curcumin prevents AsChinese medicine · 2021Article
- Health Effects Associated With Pre- and Perinatal Exposure to Arsenic.Frontiers in genetics · 2021Review
- Statistical Assessment of Toxic and Essential Metals in the Serum of Female Patients with Lung Carcinoma from Pakistan.Biological trace element research · 2020Article
- 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
- Targeted Quantitative Proteomics Revealed Arsenite-induced Proteasomal Degradation of RhoB in Fibroblast Cells.Chemical research in toxicology · 2019Article
- Long-term exposure of immortalized keratinocytes to arsenic induces EMT, impairs differentiation in organotypic skin models and mimics aspects of human skin derangements.Archives of toxicology · 2018Article
- Selective cysteine modification of metal-free human metallothionein 1a and its isolated domain fragments: Solution structural properties revealed via ESI-MS.Protein science : a publication of the Protein Society · 2017Article
- Residue Modification and Mass Spectrometry for the Investigation of Structural and Metalation Properties of Metallothionein and Cysteine-Rich Proteins.International journal of molecular sciences · 2017Review
- Oncogenomic disruptions in arsenic-induced carcinogenesis.Oncotarget · 2017Review
- Genome-wide DNA methylation reprogramming in response to inorganic arsenic links inhibition of CTCF binding, DNMT expression and cellular transformation.Scientific reports · 2017Article
- Silencing KRAS Overexpression in Cadmium-Transformed Prostate Epithelial Cells Mitigates Malignant Phenotype.Chemical research in toxicology · 2016Article
- Chronic arsenic trioxide exposure leads to enhanced aggressiveness via Met oncogene addiction in cancer cells.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Inorganic arsenic is a human lung carcinogen. We studied the ability of chronic inorganic arsenic (2 μM; as sodium arsenite) exposure to induce a cancer phenotype in the immortalized, non-tumorigenic human lung peripheral epithelial cell line, HPL-1D. After 38 weeks of continuous arsenic exposure, secreted matrix metalloproteinase-2 (MMP2) activity increased to over 200% of control, levels linked to arsenic-induced cancer phenotypes in other cell lines. The invasive capacity of these chronic arsenic-treated lung epithelial (CATLE) cells increased to 320% of control and colony formation increased to 280% of control. CATLE cells showed enhanced proliferation in serum-free media indicative of autonomous growth. Compared to control cells, CATLE cells showed reduced protein expression of the tumor suppressor gene PTEN (decreased to 26% of control) and the putative tumor suppressor gene SLC38A3 (14% of control). Morphological evidence of epithelial-to-mesenchymal transition (EMT) occurred in CATLE cells together with appropriate changes in expression of the EMT markers vimentin (VIM; increased to 300% of control) and e-cadherin (CDH1; decreased to 16% of control). EMT is common in carcinogenic transformation of epithelial cells. CATLE cells showed increased KRAS (291%), ERK1/2 (274%), phosphorylated ERK (p-ERK; 152%), and phosphorylated AKT1 (p-AKT1; 170%) protein expression. Increased transcript expression of metallothioneins, MT1A and MT2A and the stress response genes HMOX1 (690%) and HIF1A (247%) occurred in CATLE cells possibly in adaptation to chronic arsenic exposure. Thus, arsenic induced multiple cancer cell characteristics in human peripheral lung epithelial cells. This model may be useful to assess mechanisms of arsenic-induced lung cancer.
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