ArticleToxicology and applied pharmacology2015
Human bronchial epithelial BEAS-2B cells, an appropriate in vitro model to study heavy metals induced carcinogenesis.
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 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.
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- Curcumin modulates NF-κB and Nrf2 pathways to mitigate inflammation, oxidative stress, and virulence in Pseudomonas aeruginosa-infected bronchial epithelial cells.Archives of microbiology · 2026Article
- An AOP-Based Integrated In Vitro and In Vivo Assessment of the Non-Genotoxic Carcinogenic Potential of Multi-Walled Carbon Nanotubes.Nanomaterials (Basel, Switzerland) · 2026Article
- Impact of ethanol as a vehicle for water-insoluble pollutants in BEAS-2B cell toxicity assays.Toxicology mechanisms and methods · 2025Article
- Unraveling cellular dynamic changes in tumor evolution induced by long-term low dose-rate radiation.British journal of cancer · 2025Article
- Precise modulation of BRG1 levels reveals features of mSWI/SNF dosage sensitivity.Nature genetics · 2025Article
- Dysregulation of mRNA expression by hsa-miR-186 overexpression in arsenic-induced skin carcinogenesis.Toxicology and applied pharmacology · 2025Article
- Nrf2/cyclooxygenase 2 signaling in Cr(VI)-induced carcinogenesis.Ecotoxicology and environmental safety · 2025Article
- Epstein-Barr Virus BARF1 Is Expressed in Lung Cancer and Is Associated with Cancer Progression.Cells · 2024Article
- Acute exposure to dihydroxyacetone promotes genotoxicity and chromosomal instability in lung, cardiac, and liver cell models.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Novel Ultrasound-Responsive Amyloid Formulation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Effects of the SEMA4B gene on hexavalent chromium [Cr(VI)]-induced malignant transformation of human bronchial epithelial cells.Toxicology research · 2024Article
- In silico model development and optimization of in vitro lung cell population growth.PloS one · 2024Article
- Characterization of histone chaperone MCM2 as a key regulator in arsenic-induced depletion of H3.3 at genomic loci.Toxicology and applied pharmacology · 2023Article
- In Vitro Cell Transformation Assays: A Valuable Approach for Carcinogenic Potentiality Assessment of Nanomaterials.International journal of molecular sciences · 2023Review
- Dissection of Cancer Mutational Signatures with Individual Components of Cigarette Smoking.Chemical research in toxicology · 2023Article
- The β-Blocker Carvedilol Prevents Benzo(a)pyrene-Induced Lung Toxicity, Inflammation and Carcinogenesis.Cancers · 2023Article
- The pivotal regulatory factor circBRWD1 inhibits arsenic exposure-induced lung cancer occurrence by binding mRNA and regulating its stability.Molecular therapy oncolytics · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Occupational and environmental exposure to arsenic (III) and chromium VI (Cr(VI)) have been confirmed to cause lung cancer. Mechanisms of these metals carcinogenesis are still under investigation. Selection of cell lines to be used is essential for the studies. Human bronchial epithelial BEAS-2B cells are the cells to be utilized by most of scientists. However, due to p53 missense mutation (CCG→TCG) at codon 47 and the codon 72 polymorphism (CGC→CCC) in BEAS-2B cells, its usage has frequently been questioned. The present study has examined activity and expression of 53 and its downstream target protein p21 upon acute or chronic exposure of BEAS-2B cells to arsenic and Cr(VI). The results show that short-term exposure of BEAS-2B cells to arsenic or Cr(VI) was able to activate both p53 and p21. Chronic exposure of BEAS-2B cells to these two metals caused malignant cell transformation and tumorigenesis. In arsenic-transformed BEAS-2B cells reductions in p53 promoter activity, mRNA expression, and phosphorylation of p53 at Ser392 were observed, while the total p53 protein level remained the same compared to those in passage-matched parent ones. p21 promoter activity and expression were decreased in arsenic-transformed cells. Cr(VI)-transformed cells exhibit elevated p53 promoter activity, mRNA expression, and phosphorylation at Ser15, but reduced phosphorylation at Ser392 and total p53 protein level compared to passage-matched parent ones. p21 promoter activity and expression were elevated in Cr(VI)-transformed cells. These results demonstrate that p53 is able to respond to exposure of arsenic or Cr(VI), suggesting that BEAS-2B cells are an appropriate in vitro model to investigate arsenic or Cr(VI) induced lung cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.