ArticleBiochemical and biophysical research communications2015
Role of reactive oxygen species in arsenic-induced transformation of human lung bronchial epithelial (BEAS-2B) cells.
Article in Biochemical and biophysical research communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30 citing papers in PubMed, 67 citations in OpenAlex.
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- Connections between endoplasmic reticulum stress-associated unfolded protein response, mitochondria, and autophagy in arsenic-induced carcinogenesis.Seminars in cancer biology · 2021Review
- Chemopreventive Role of Black Tea Extract in Swiss Albino Mice Exposed to Inorganic Arsenic.Asian Pacific journal of cancer prevention : APJCP · 2021Article
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- Paradoxical effects of arsenic in the lungs.Environmental health and preventive medicine · 2021Review
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- Overexpression of hsa-miR-186 induces chromosomal instability in arsenic-exposed human keratinocytes.Toxicology and applied pharmacology · 2019Article
- Constitutive Activation of NAD-Dependent Sirtuin 3 Plays an Important Role in Tumorigenesis of Chromium(VI)-Transformed Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Grape seed proanthocyanidin extract alleviates arsenic-induced lung damage through NF-κB signaling.Experimental biology and medicine (Maywood, N.J.) · 2019Article
- Metals and Mechanisms of Carcinogenesis.Annual review of pharmacology and toxicology · 2019Review
- Arsenic-Induced Carcinogenesis: The Impact of miRNA Dysregulation.Toxicological sciences : an official journal of the Society of Toxicology · 2018Review
- Fetal bovine serum induces sustained, but reversible, epithelial-mesenchymal transition in the BEAS-2B cell line.Toxicology in vitro : an international journal published in association with BIBRA · 2018Article
- Oxidative Stress and Metabolic Reprogramming in Cr(VI) Carcinogenesis.Current opinion in toxicology · 2018Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Arsenic is an environmental carcinogen, its mechanisms of carcinogenesis remain to be investigated. Reactive oxygen species (ROS) are considered to be important. A previous study (Carpenter et al., 2011) has measured ROS level in human lung bronchial epithelial (BEAS-2B) cells and arsenic-transformed BEAS-2B cells and found that ROS levels were higher in transformed cells than that in parent normal cells. Based on these observations, the authors concluded that cell transformation induced by arsenic is mediated by increased cellular levels of ROS. This conclusion is problematic because this study only measured the basal ROS levels in transformed and parent cells and did not investigate the role of ROS in the process of arsenic-induced cell transformation. The levels of ROS in arsenic-transformed cells represent the result and not the cause of cell transformation. Thus question concerning whether ROS are important in arsenic-induced cell transformation remains to be answered. In the present study, we used expressions of catalase (antioxidant against H2O2) and superoxide dismutase 2 (SOD2, antioxidant against O2(-)) to decrease ROS level and investigated their role in the process of arsenic-induced cell transformation. Our results show that inhibition of ROS by antioxidant enzymes decreased arsenic-induced cell transformation, demonstrating that ROS are important in this process. We have also shown that in arsenic-transformed cells, ROS generation was lower and levels of antioxidants are higher than those in parent cells, in a disagreement with the previous report. The present study has also shown that the arsenic-transformed cells acquired apoptosis resistance. The inhibition of catalase to increase ROS level restored apoptosis capability of arsenic-transformed BEAS-2B cells, further showing that ROS levels are low in these cells. The apoptosis resistance due to the low ROS levels may increase cells proliferation, providing a favorable environment for tumorigenesis of arsenic-transformed cells.
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