ArticleScientific reports2017
Identification of ARNT-regulated BIRC3 as the target factor in cadmium renal toxicity.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 22 citations in OpenAlex.
- Molecular Mechanisms of Cadmium-Induced Toxicity and Its Modification.International journal of molecular sciences · 2025Review
- Cadmium Toxicity Is Regulated by Peroxisome Proliferator-Activated Receptor δ in Human Proximal Tubular Cells.International journal of molecular sciences · 2022Article
- Baculoviral inhibitor of apoptosis protein repeat-containing protein 3 delays early Wallerian degeneration after sciatic nerve injury.Neural regeneration research · 2022Article
- Contrasting functions of the epithelial‑stromal interaction 1 gene, in human oral and lung squamous cell cancers.Oncology reports · 2022Article
- CLDN1 regulates trophoblast apoptosis and proliferation in preeclampsia.Reproduction (Cambridge, England) · 2021Article
- Methylmercury toxic mechanism related to protein degradation and chemokine transcription.Environmental health and preventive medicine · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
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Abstract
Cadmium (Cd) is an environmental contaminant that exhibits renal toxicity. The target transcription factors involved in Cd renal toxicity are still unknown. In this study, we demonstrated that Cd decreased the activity of the ARNT transcription factor, and knockdown of ARNT significantly decreased the viability of human proximal tubular HK-2 cells. Microarray analysis in ARNT knockdown cells revealed a decrease in the expression of a number of genes, including a known apoptosis inhibitor, BIRC3, whose gene and protein expression level was also decreased by Cd treatment. Although the BIRC family consists of 8 members, Cd suppressed only BIRC3 gene expression. BIRC3 is known to suppress apoptosis through the inhibition effect on caspase-3. Knockdown of BIRC3 by siRNA as well as Cd treatment increased the level of active caspase-3. Moreover, knockdown of BIRC3 not only triggered cell toxicity and apoptosis but also strengthened Cd toxicity in HK-2 cells. Meanwhile, the activation of caspase-3 by suppression of BIRC3 gene expression was mostly specific to Cd and to proximal tubular cells. These results suggest that Cd induces apoptosis through the inhibition of ARNT-regulated BIRC3 in human proximal tubular cells.
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