ArticleEnvironmental health perspectives2002
DDT and its metabolites alter gene expression in human uterine cell lines through estrogen receptor-independent mechanisms.
Article in Environmental health perspectives, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 63 citations in OpenAlex.
- Insecticides and testicular health: mechanisms of injury and protective natural products.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- p,p'-DDT induces apoptosis in human endometrial stromal cells via the PI3K/AKT pathway and oxidative stress.Clinical and experimental reproductive medicine · 2024Article
- Cross-species metabolomic analysis of tau- and DDT-related toxicity.PNAS nexus · 2022Article
- Agrochemicals with estrogenic endocrine disrupting properties: Lessons Learned?Molecular and cellular endocrinology · 2020Review
- Edible Plant Oil: Global Status, Health Issues, and Perspectives.Frontiers in plant science · 2020Review
- Endocrine Disruptors Leading to Obesity and Related Diseases.International journal of environmental research and public health · 2017Review
- Endocrine disruption of the epigenome: a breast cancer link.Endocrine-related cancer · 2014Review
- Assessment of organochlorine pesticides and plasticisers in the Selangor River basin and possible pollution sources.Environmental monitoring and assessment · 2013Article
- Antiestrogenic activity of flavonoid phytochemicals mediated via the c-Jun N-terminal protein kinase pathway. Cell-type specific regulation of estrogen receptor alpha.The Journal of steroid biochemistry and molecular biology · 2012Article
- The organochlorine o,p'-DDT plays a role in coactivator-mediated MAPK crosstalk in MCF-7 breast cancer cells.Environmental health perspectives · 2012Article
- Gαo potentiates estrogen receptor α activity via the ERK signaling pathway.The Journal of endocrinology · 2012Article
- Environmental signaling and reproduction: a comparative biological and chemical perspective.Molecular and cellular endocrinology · 2012Review
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- Estrogenic activity of coumestrol, DDT, and TCDD in human cervical cancer cells.International journal of environmental research and public health · 2010Article
- Increased expression of histone proteins during estrogen-mediated cell proliferation.Environmental health perspectives · 2009Article
- Organochlorine-mediated potentiation of the general coactivator p300 through p38 mitogen-activated protein kinase.Carcinogenesis · 2009Article
- Low doses of bisphenol A and diethylstilbestrol impair Ca2+ signals in pancreatic alpha-cells through a nonclassical membrane estrogen receptor within intact islets of Langerhans.Environmental health perspectives · 2005Article
- Disentangling the molecular mechanisms of action of endogenous and environmental estrogens.Pflugers Archiv : European journal of physiology · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endocrine-disrupting organochlorines, such as the pesticide dichlorodiphenyltrichloroethane (DDT), bind to and activate estrogen receptors (ERs), thereby eliciting estrogen-like effects. Although ERs function predominantly through activation of transcription via estrogen-responsive elements, both ERs, alpha and ss, can interact with various transcription factors such as activator protein-1 (AP-1). Additionally, estrogens may regulate early signaling events, suggesting that the biological effects of environmental estrogens may not be mediated through classic ER (alpha and ss) activity alone. We hypothesized that known environmental estrogens, such as DDT and its metabolites, activate AP-1-mediated gene transactivation through both ER-dependent and ER-independent means. Using two Ishikawa human endometrial adenocarcinoma cell line variants that we confirmed to be estrogen responsive [Ishikawa(+)] and estrogen unresponsive [Ishikawa(-)], we generated stably transfected AP-1 luciferase cell lines to identify the role of an estrogen-responsive mechanism in AP-1-mediated gene expression by various stimuli. Our results demonstrate that DDT and dichlorodiphenyldichloroethane (DDD) were the most potent activators of AP-1 activity; 2,2-bis(p-chlorophenyl) acetic acid failed to activate. Although stimulated in both Ishikawa(+) and Ishikawa(-) cells by DDT and its congeners, AP-1 activation was more pronounced in the estrogen-unresponsive Ishikawa(-) cells. In addition, DDT, DDD, and dichlorodiphenyldichloroethylene (DDE) could also stimulate AP-1 activity in the estrogen-unresponsive human embryonic kidney 293 cells using a different promoter context. Thus, our data demonstrate that DDT and its metabolites activate the AP-1 transcription factor independent of ER (alpha or ss) status.
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