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- W2772035849 abstract "Cr(VI)-containing compounds are well-established lung carcinogens. Chronic exposure of the normal human epithelial cells is able to induce malignant cell transformation, the first stage of metal carcinogenesis. These Cr(VI)-transformed cells exhibit increased level of antioxidants, reduced capacity of generating reactive oxygen species (ROS), and development of apoptosis resistance, promoting tumorigenesis of Cr(VI)-transformed cells, the second stage of metal carcinogenesis. The mechanism of Cr(VI) induced carcinogenesis is still under investigation. Recent studies indicate that ROS play a positive role in the first stage while a negative role in the second stage. Transformed cells adapt metabolism to support tumor initiation and progression. Altered metabolic activities directly participate in the process of cell transformation or support a large requirement for nucleotides, amino acids, and lipids for tumor growth. In malignantly Cr(VI)-transformed cells, mitochondrial oxidative phosphorylation is defective, and pentose phosphate pathway, glycolysis, and glutaminolysis are upregulated. These metabolic reprogramming supports rapid cell proliferation and contributes to tumorigenesis of Cr(VI)-transformed cells. This article summarizes the current progress in the studies of metabolic reprogramming and Cr(VI) carcinogenesis with emphasis on the metabolic enzymes and oxidative stress related major oncogenic pathways." @default.
- W2772035849 created "2017-12-22" @default.
- W2772035849 creator A5005038385 @default.
- W2772035849 creator A5069596466 @default.
- W2772035849 creator A5088517899 @default.
- W2772035849 date "2018-04-01" @default.
- W2772035849 modified "2023-09-30" @default.
- W2772035849 title "Oxidative stress and metabolic reprogramming in Cr(VI) carcinogenesis" @default.
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- W2772035849 doi "https://doi.org/10.1016/j.cotox.2017.11.015" @default.
- W2772035849 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5858573" @default.
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- W2772035849 hasPublicationYear "2018" @default.
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