ArticleToxicological research2011
Cell Growth of BG-1 Ovarian Cancer Cells was Promoted by 4-Tert-octylphenol and 4-Nonylphenol via Downregulation of TGF-β Receptor 2 and Upregulation of c-myc.
Article in Toxicological research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed, 23 citations in OpenAlex.
- Oncogenic Potential of Bisphenol A and Common Environmental Contaminants in Human Mammary Epithelial Cells.International journal of molecular sciences · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor β (TGF-β) is involved in cellular processes including growth, differentiation, apoptosis, migration, and homeostasis. Generally, TGF-β is the inhibitor of cell cycle progression and plays a role in enhancing the antagonistic effects of many growth factors. Unlike the antiproliferative effect of TGF-β, E2, an endogeneous estrogen, is stimulating cell proliferation in the estrogen-dependent organs, which are mediated via the estrogen receptors, ERα and ERβ, and may be considered as a critical risk factor in tumorigenesis of hormone-responsive cancers. Previous researches reported the cross-talk between estrogen/ERα and TGF-β pathway. Especially, based on the E2-mediated inhibition of TGF-β signaling, we examined the inhibition effect of 4-tert-octylphenol (OP) and 4-nonylphenol (NP), which are well known xenoestrogens in endocrine disrupting chemicals (EDCs), on TGF-β signaling via semi-quantitative reverse-transcription PCR. The treatment of E2, OP, or NP resulted in the downregulation of TGF- β receptor2 (TGF-β R2) in TGF-β signaling pathway. However, the expression level of TGF-β1 and TGF- β receptor1 (TGF-β R1) genes was not altered. On the other hand, E2, OP, or NP upregulated the expression of a cell-cycle regulating gene, c-myc, which is a oncogene and a downstream target gene of TGF-β signaling pathway. As a result of downregulation of TGF-β R2 and the upregulation of c-myc, E2, OP, or NP increased cell proliferation of BG-1 ovarian cancer cells. Taken together, these results suggest that E2 and these two EDCs may mediate cancer cell proliferation by inhibiting TGF-β signaling via the downregulation of TGF-β R2 and the upregulation of c-myc oncogene. In addition, it can be inferred that these EDCs have the possibility of tumorigenesis in estrogen-responsive organs by certainly representing estrogenic effect in inhibiting TGF-β signaling.
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