ArticlePloS one2014
Prediction of the number of activated genes in multiple independent Cd(+2)- and As(+3)-induced malignant transformations of human urothelial cells (UROtsa).
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Zinc, Zinc Transporters, and Cadmium Cytotoxicity in a Cell Culture Model of Human Urothelium.Toxics · 2021Article
- Meta-analysis of gene expression profiling reveals novel basal gene signatures in MCF-10A cells transformed with cadmium.Oncotarget · 2020Article
- Article
- The expression of keratin 6 is regulated by the activation of the ERK1/2 pathway in arsenite transformed human urothelial cells.Toxicology and applied pharmacology · 2017Article
- 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
- Loss of N-Cadherin Expression in Tumor Transplants Produced From As+3- and Cd+2-Transformed Human Urothelial (UROtsa) Cell Lines.PloS one · 2016Article
- Chronic inorganic arsenic exposure in vitro induces a cancer cell phenotype in human peripheral lung epithelial cells.Toxicology and applied pharmacology · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMany toxic environmental agents such as cadmium and arsenic are found to be epidemiologically linked to increasing rates of cancers. In vitro studies show that these toxic agents induced malignant transformation in human cells. It is not clear whether such malignant transformation induced by a single toxic agent is driven by a common set of genes. Although the advancement of high-throughput technology has facilitated the profiling of global gene expression, it remains a question whether the sample size is sufficient to identify this common driver gene set.
resultsWe have developed a statistical method, SOFLR, to predict the number of common activated genes using a limited number of microarray samples. We conducted two case studies, cadmium and arsenic transformed human urothelial cells. Our method is able to precisely predict the number of stably induced and repressed genes and the number of samples to identify the common activated genes. The number of independent transformed isolates required for identifying the common activated genes is also estimated. The simulation study further validated our method and identified the important parameters in this analysis.
conclusionsOur method predicts the degree of similarity and diversity during cell malignant transformation by a single toxic agent. The results of our case studies imply the existence of common driver and passenger gene sets in toxin-induced transformation. Using a pilot study with small sample size, this method also helps microarray experimental design by determining the number of samples required to identify the common activated gene set.
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