ArticlePloS one2013
An alkylphenol mix promotes seminoma derived cell proliferation through an ERalpha36-mediated mechanism.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 42 citations in OpenAlex.
- Implications of hormonal carcinogenesis for transgender and gender-diverse people undergoing gender-affirming hormone therapy: an up-to-date review.BMJ oncology · 2024Review
- Article
- The Role of ERα36 in Development and Tumor Malignancy.International journal of molecular sciences · 2020Review
- Oncogenic Potential of Bisphenol A and Common Environmental Contaminants in Human Mammary Epithelial Cells.International journal of molecular sciences · 2020Article
- GPER and Testicular Germ Cell Cancer.Frontiers in endocrinology · 2020Review
- Dual Epigenetic Regulation of ERα36 Expression in Breast Cancer Cells.International journal of molecular sciences · 2019Article
- Chronic low-dose exposure to a mixture of environmental endocrine disruptors induces microRNAs/isomiRs deregulation in mouse concomitant with intratesticular estradiol reduction.Scientific reports · 2017Article
- Low-Dose Alkylphenol Exposure Promotes Mammary Epithelium Alterations and Transgenerational Developmental Defects, But Does Not Enhance Tumorigenic Behavior of Breast Cancer Cells.Frontiers in endocrinology · 2017Article
- Mammary epithelial cell phenotype disruption in vitro and in vivo through ERalpha36 overexpression.PloS one · 2017Article
- Molecular biology of testicular germ cell tumors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2016Review
- Role of ER-α36 in breast cancer by typical xenoestrogens.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
- From ERα66 to ERα36: a generic method for validating a prognosis marker of breast tumor progression.BMC systems biology · 2015Article
- Endocrine-disrupting Chemicals: Review of Toxicological Mechanisms Using Molecular Pathway Analysis.Journal of cancer prevention · 2015Review
- Reporter Cell Lines for the Characterization of the Interactions between Human Nuclear Receptors and Endocrine Disruptors.Frontiers in endocrinology · 2015Review
- The many faces of estrogen signaling.Biochemia medica · 2014Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long chain alkylphenols are man-made compounds still present in industrial and agricultural processes. Their main use is domestic and they are widespread in household products, cleansers and cosmetics, leading to a global environmental and human contamination. These molecules are known to exert estrogen-like activities through binding to classical estrogen receptors. In vitro, they can also interact with the G-protein coupled estrogen receptor. Testicular germ cell tumor etiology and progression are proposed to be stimulated by lifelong estrogeno-mimetic exposure. We studied the transduction signaling pathways through which an alkyphenol mixture triggers testicular cancer cell proliferation in vitro and in vivo. Proliferation assays were monitored after exposure to a realistic mixture of 4-tert-octylphenol and 4-nonylphenol of either TCam-2 seminoma derived cells, NT2/D1 embryonal carcinoma cells or testis tumor in xenografted nude mice. Specific pharmacological inhibitors and gene-silencing strategies were used in TCam-2 cells in order to demonstrate that the alkylphenol mix triggers CREB-phosphorylation through a rapid, ERα36-PI3kinase non genomic pathway. Microarray analysis of the mixture target genes revealed that this pathway can modulate the expression of the DNA-methyltransferase-3 (Dnmt3) gene family which is involved in DNA methylation control. Our results highlight a key role for ERα36 in alkylphenol non genomic signaling in testicular germ cell tumors. Hence, ERα36-dependent control of the epigenetic status opens the way for the understanding of the link between endocrine disruptor exposure and the burden of hormone sensitive cancers.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.