ArticleEnvironmental health perspectives2007
Acquisition of apoptotic resistance in cadmium-transformed human prostate epithelial cells: Bcl-2 overexpression blocks the activation of JNK signal transduction pathway.
Article in Environmental health perspectives, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 57 citations in OpenAlex.
- From environmental exposure to retinal pathology: epidemiological and mechanistic insights into multi-metal driven ocular diseases.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
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- Interaction between NF-κB and PLAC8 impairs autophagy providing a survival advantage to prostate cells transformed by cadmium.Science advances · 2025Article
- Mechanisms of Heavy Metal Cadmium (Cd)-Induced Malignancy.Biological trace element research · 2025Review
- Heavy metals: toxicity and human health effects.Archives of toxicology · 2025Review
- UV-C Exposure Enhanced the CdMicroorganisms · 2024Article
- The dynamic face of cadmium-induced Carcinogenesis: Mechanisms, emerging trends, and future directions.Current research in toxicology · 2024Review
- Toxic Mechanisms of Five Heavy Metals: Mercury, Lead, Chromium, Cadmium, and Arsenic.Frontiers in pharmacology · 2021Review
- Mode of action-based risk assessment of genotoxic carcinogens.Archives of toxicology · 2020Review
- Neuroprotective Effects of Polydeoxyribonucleotide in a Murine Model of Cadmium Toxicity.Oxidative medicine and cellular longevity · 2018Article
- Induction of Plac8 promotes pro-survival function of autophagy in cadmium-induced prostate carcinogenesis.Cancer letters · 2017Article
- Silencing KRAS Overexpression in Cadmium-Transformed Prostate Epithelial Cells Mitigates Malignant Phenotype.Chemical research in toxicology · 2016Article
- BH4 domain of Bcl-2 as a novel target for cancer therapy.Drug discovery today · 2016Review
- Protective effects of Lactobacillus plantarum CCFM8610 against chronic cadmium toxicity in mice indicate routes of protection besides intestinal sequestration.Applied and environmental microbiology · 2014Article
- A review of molecular events of cadmium-induced carcinogenesis.Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer · 2014Review
- Article
- Role of oxidative stress in cadmium toxicity and carcinogenesis.Toxicology and applied pharmacology · 2009Review
- Transcriptome analyses in normal prostate epithelial cells exposed to low-dose cadmium: oncogenic and immunomodulations involving the action of tumor necrosis factor.Environmental health perspectives · 2008Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundWe have recently shown that cadmium can induce malignant transformation of the human prostate epithelial cell line (RWPE-1) and that these cadmium-transformed prostate epithelial (CTPE) cells acquire apoptotic resistance concurrently with malignant phenotype.
objectiveThe present study was designed to define the mechanism of acquired apoptotic resistance in CTPE cells.
methodsVarious molecular events associated with apoptosis were assessed in control and CTPE cells that were obtained after 8 weeks of continuous cadmium exposure.
resultsCompared with control, CTPE cells showed a generalized resistance to apoptosis induced by cadmium, cisplatin, or etoposide. Signal-regulated mitogen-activated protein kinases, extracellular signal-regulated kinases 1 and 2, c-Jun N-terminal kinases (JNK1 and JNK2), and p38 were phosphorylated in a cadmium concentration-dependent fashion in CTPE and control cells. However, phosphorylated JNK1/2 levels and JNK kinase activity were much lower in CTPE cells. The pro-apoptotic gene Bax showed lower transcript and protein levels, whereas the anti-apoptotic gene Bcl-2 showed higher levels in CTPE cells. The ratio of Bcl-2/Bax, a key determinant in apoptotic commitment, increased more than 4-fold in CTPE cells. In Bcl-2-transfected PT-67 cells, phosphorylated JNK1/2 levels were much lower after apoptogenic stimulus, and apoptosis induced by cadmium or etoposide was reduced compared with control. Mutation of tyrosine to serine at the 21st amino acid of the Bcl-2 protein BH4 domain resulted in a loss both of suppression of JNK1/2 phosphorylation and its anti-apoptotic function.
conclusionsCTPE cells become resistant to apoptosis during malignant transformation, and disruption of the JNK pathway and Bcl-2 overexpression play important roles in this resistance. Bcl-2 BH4 domain is required for modulating JNK phosphorylation and anti-apoptotic function.
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Registered trials
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