ArticleToxicology letters2012
Increased neuron specific enolase expression by urothelial cells exposed to or malignantly transformed by exposure to Cd²⁺ or As³⁺.
Article in Toxicology letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- BeyondMolecular therapy oncolytics · 2023Review
- Specific activation of glycolytic enzyme enolase 2 in BRAF V600E-mutated colorectal cancer.Cancer science · 2021Article
- Multifunctional neuron-specific enolase: its role in lung diseases.Bioscience reports · 2019Review
- NSE from diffuse large B-cell lymphoma cells regulates macrophage polarization.Cancer management and research · 2019Article
- Elevated connexin 43 expression in arsenite-and cadmium-transformed human bladder cancer cells, tumor transplants and selected high grade human bladder cancers.Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie · 2016Article
- Comparative proteomic analysis of malignant pleural mesothelioma: Focusing on the biphasic subtype.EuPA open proteomics · 2016Article
- Loss of N-Cadherin Expression in Tumor Transplants Produced From As+3- and Cd+2-Transformed Human Urothelial (UROtsa) Cell Lines.PloS one · 2016Article
- Gamma-enolase: a well-known tumour marker, with a less-known role in cancer.Radiology and oncology · 2015Review
- Epigenetic effects of cadmium in cancer: focus on melanoma.Current genomics · 2014Article
- Glycolytic genes in cancer cells are more than glucose metabolic regulators.Journal of molecular medicine (Berlin, Germany) · 2014Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Neuron specific enolase (ENO2, γ-enolase) is a biomarker used to help identify neuroendocrine differentiation in tumors. This laboratory has shown that ENO2 might be a biomarker for exposure to cadmium and arsenite. In this study these observations are extended to the urothelial cell, where environmental exposures are strongly linked to urothelial cancer. The UROtsa urothelial cell line and its Cd²⁺- and As³⁺-transformed counterparts were used as the model. Acute exposure of the UROtsa cells to both As³⁺- and Cd²⁺-caused significant increases in ENO2 expression. Treatment with the histone deacetlyase inhibitor was also shown to significantly increase the expression of ENO2 mRNA. The expression of ENO2 was significantly elevated in the Cd²⁺- and As³⁺-transformed UROtsa cells and tumor transplants. In contrast, ENO1, was unaffected by exposure to As³⁺ or Cd²⁺. Immunofluorescence showed ENO2 associated with both the nucleus and cytoplasm and cytoplasmic ENO2 co-localized with ENO1. The findings extend the evidence suggesting a link between As³⁺ and Cd²⁺ exposure and neuroendocrine differentiation in tumors. The results suggest that ENO2 might be a biomarker of human exposure to Cd²⁺ and As³⁺ that operates through histone modification.
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