ArticleThe Biochemical journal2012
Oestrogen causes ATBF1 protein degradation through the oestrogen-responsive E3 ubiquitin ligase EFP.
Article in The Biochemical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- TRIM Protein Superfamily in Breast Cancer: Yin and Yang.Biochemical genetics · 2026Review
- TRIM25 degrades BRD7 protein stability through the ubiquitin proteasome pathway to promote breast cancer progression and paclitaxel resistance by activating YB1/Bcl-2 transcription axis.Cell death & disease · 2025Article
- Bisphenol a Disrupts Steroidogenesis and Induces Apoptosis in Human Granulosa Cells Cultured In Vitro.International journal of molecular sciences · 2025Article
- Ubiquitination Enzymes in Cancer, Cancer Immune Evasion, and Potential Therapeutic Opportunities.Cells · 2025Review
- The SUMOylation and ubiquitination crosstalk in cancer.Journal of cancer research and clinical oncology · 2023Review
- Genomic Signatures Associated with Transitions to Viviparity in Cyprinodontiformes.Molecular biology and evolution · 2023Article
- The moonlighting function of glycolytic enzyme enolase-1 promotes choline phospholipid metabolism and tumor cell proliferation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- ATBF1 is a potential diagnostic marker of histological grade and functions via WNT5A in breast cancer.BMC cancer · 2022Article
- Elucidation of TRIM25 ubiquitination targets involved in diverse cellular and antiviral processes.PLoS pathogens · 2022Article
- Review
- E3 ligase TRIM25 ubiquitinates RIP3 to inhibit TNF induced cell necrosis.Cell death and differentiation · 2021Article
- TRIM25: A central factor in breast cancer.World journal of clinical oncology · 2021Review
- circNDUFB2 inhibits non-small cell lung cancer progression via destabilizing IGF2BPs and activating anti-tumor immunity.Nature communications · 2021Article
- SUMOylation of the transcription factor ZFHX3 at Lys-2806 requires SAE1, UBC9, and PIAS2 and enhances its stability and function in cell proliferation.The Journal of biological chemistry · 2020Article
- ZFHX3 is indispensable for ERβ to inhibit cell proliferation via MYC downregulation in prostate cancer cells.Oncogenesis · 2019Article
- Sex Hormones in Acquired Immunity and Autoimmune Disease.Frontiers in immunology · 2018Review
- Efp promotes in vitro and in vivo growth of endometrial cancer cells along with the activation of nuclear factor-κB signaling.PloS one · 2018Article
- TRIM25 Is Required for the Antiviral Activity of Zinc Finger Antiviral Protein.Journal of virology · 2017Article
- Article
- A complex insertion/deletion polymorphism in the compositionally biased region of the ZFHX3 gene in patients with coronary heart disease in a Chinese population.International journal of clinical and experimental medicine · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We reported previously that the tumour suppressor ATBF1 (AT motif-binding factor 1) formed an autoregulatory feedback loop with oestrogen-ERα (oestrogen receptor α) signalling to regulate oestrogen-dependent cell proliferation in breast cancer cells. In this loop ATBF1 inhibits the function of oestrogen-ERα signalling, whereas ATBF1 protein levels are fine-tuned by oestrogen-induced transcriptional up-regulation as well as UPP (ubiquitin-proteasome pathway)-mediated protein degradation. In the present study we show that EFP (oestrogen-responsive finger protein) is an E3 ubiquitin ligase mediating oestrogen-induced ATBF1 protein degradation. Knockdown of EFP increases ATBF1 protein levels, whereas overexpression of EFP decreases ATBF1 protein levels. EFP interacts with and ubiquitinates ATBF1 protein. Furthermore, we show that EFP is an important factor in oestrogen-induced ATBF1 protein degradation in which some other factors are also involved. In human primary breast tumours the levels of ATBF1 protein are positively correlated with the levels of EFP protein, as both are directly up-regulated ERα target gene products. However, the ratio of ATBF1 protein to EFP protein is negatively correlated with EFP protein levels. Functionally, ATBF1 antagonizes EFP-mediated cell proliferation. These findings not only establish EFP as the E3 ubiquitin ligase for oestrogen-induced ATBF1 protein degradation, but further support the autoregulatory feedback loop between ATBF1 and oestrogen-ERα signalling and thus implicate ATBF1 in oestrogen-dependent breast development and carcinogenesis.
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