ArticleCellular signalling2012
SnoN oncoprotein enhances estrogen receptor-α transcriptional activity.
Article in Cellular signalling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Sumoylated SnoN interacts with HDAC1 and p300/CBP to regulate EMT-associated phenotypes in mammary organoids.Cell death & disease · 2023Article
- Review
- Herbal compound 861 prevents hepatic fibrosis by inhibiting the TGF-β1/Smad/SnoN pathway in bile duct-ligated rats.BMC complementary and alternative medicine · 2018Article
- The influence of SnoN gene silencing by siRNA on the cell proliferation and apoptosis of human pancreatic cancer cells.Diagnostic pathology · 2015Article
- Article
- Regulation of estrogen receptor signaling in breast carcinogenesis and breast cancer therapy.Cellular and molecular life sciences : CMLS · 2014Article
- SnoN signaling in proliferating cells and postmitotic neurons.FEBS letters · 2012Review
- Chemotherapeutic Targeting of the Transforming Growth Factor-β Pathway in Breast Cancers.Breast cancer managementArticle
- Transcriptional cofactors Ski and SnoN are major regulators of the TGF-β/Smad signaling pathway in health and disease.Signal transduction and targeted therapyArticle
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2 authors.
Funding
Abstract
Estrogen receptor-α (ERα) and transforming growth factor-beta (TGF-β) signaling pathways are essential regulators during mammary gland development and tumorigenesis. Ski-related novel gene (SnoN) is an oncoprotein and a negative feedback inhibitor of TGF-β signaling. We have previously reported that low expression of SnoN in ERα positive breast carcinomas is associated with favorable prognosis (Zhang et al. Cancer Res. (2003) 63, 5005-5010). Here we have studied the mechanism of a possible cross-talk between ERα and SnoN. We find that SnoN interacts with the estrogen-activated form of ERα in the nucleus. SnoN contains two highly conserved nuclear receptor binding LxxLL-like motifs and we show that mutations in these motifs reduce the interaction of SnoN with ERα. Over-expression of SnoN enhanced the transcriptional activity of ERα in estrogen response element (ERE)-reporter assays, augmented the expression of several ERα target genes and increased the proliferation of MCF7 breast carcinoma cells in an estrogen-dependent manner. Chromatin immunoprecipitation demonstrated that SnoN interacts with ERα at the TTF1 (pS2) gene promoter. Conversely, silencing of SnoN reduced both ERE-reporter activity and the expression of ERα target genes in MCF7 and T-47D breast cancer cells. Histone deacetylase inhibition increased the level of SnoN and SnoN-dependent enhancement of ERα-dependent transcription and SnoN supported the recruitment of p300 histone acetylase to ERα. This study reveals a novel mechanism that interconnects ERα and TGF-β signaling pathways by SnoN. Accordingly, the results indicate that high SnoN level promotes ERα signaling and possibly breast cancer progression.
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