ArticleThe Biochemical journal2011
Oestrogen causes degradation of KLF5 by inducing the E3 ubiquitin ligase EFP in ER-positive breast cancer cells.
Article in The Biochemical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- A Novel Emerin/Nesprin-3 Interaction Mediates Nuclear Size Changes Induced by Oncogenic KRAS in Pancreatic Cancer Cells.Molecular and cellular biology · 2026Article
- Krüppel-Like Factors Modulate Susceptibility To Neuropsychiatric Disorders.Molecular neurobiology · 2025Review
- TRIM25, TRIM28 and TRIM59 and Their Protein Partners in Cancer Signaling Crosstalk: Potential Novel Therapeutic Targets for Cancer.Current issues in molecular biology · 2024Review
- Methionine orchestrates the metabolism vulnerability in cisplatin resistant bladder cancer microenvironment.Cell death & disease · 2023Article
- New insights into KLFs and SOXs in cancer pathogenesis, stemness, and therapy.Seminars in cancer biology · 2023Review
- Review
- Krüppel-like factor (KLF)5: An emerging foe of cardiovascular health.Journal of molecular and cellular cardiology · 2022Review
- TRIM25: A central factor in breast cancer.World journal of clinical oncology · 2021Review
- The roles and regulation of the KLF5 transcription factor in cancers.Cancer science · 2021Review
- circNDUFB2 inhibits non-small cell lung cancer progression via destabilizing IGF2BPs and activating anti-tumor immunity.Nature communications · 2021Article
- TRK-Fused Gene (TFG), a protein involved in protein secretion pathways, is an essential component of the antiviral innate immune response.PLoS pathogens · 2021Article
- USP3 promotes breast cancer cell proliferation by deubiquitinating KLF5.The Journal of biological chemistry · 2019Article
- Treatment with a brain-selective prodrug of 17β-estradiol improves cognitive function in Alzheimer's disease mice by regulating klf5-NF-κB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2019Article
- HDAC-mediated deacetylation of KLF5 associates with its proteasomal degradation.Biochemical and biophysical research communications · 2018Article
- TRIM25 enhances cell growth and cell survival by modulating p53 signals via interaction with G3BP2 in prostate cancer.Oncogene · 2018Article
- 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
- DNMT1-maintained hypermethylation of Krüppel-like factor 5 involves in the progression of clear cell renal cell carcinoma.Cell death & disease · 2017Article
- Article
- Estrogen Exhibits a Biphasic Effect on Prostate Tumor Growth through the Estrogen Receptor β-KLF5 Pathway.Molecular and cellular biology · 2016Article
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6 authors at 1 institution in 1 country.
Funding
Abstract
KLF5 (Krüppel-like factor 5) is a multifunctional transcription factor involved in cell proliferation, differentiation and carcinogenesis. In addition to frequent inactivation in different types of human cancers, including breast cancer, KLF5 has been identified as an essential co-factor for the TGF-β (transforming growth factor β) tumour suppressor. In our previous study demonstrating a negative regulation of ER (oestrogen receptor α) function by KLF5 in breast cancer cells [Guo, Dong, Zhao, Sun, Li and Dong (2010) Int. J. Cancer 126, 81-89], we noticed that oestrogen reduced the protein level of KLF5. In the present study, we have tested whether and how oestrogen/ER signalling regulates KLF5 protein. We found that oestrogen caused the degradation of KLF5 protein, and the degradation was sensitive to proteasome inhibitors, but not other inhibitors. The oestrogen-inducible E3 ligase EFP (oestrogen-responsive finger protein) was identified as a key player in oestrogen-mediated degradation of KLF5, as knockdown and overexpression of EFP increased and decreased KLF5 protein levels respectively, and the decrease continued even when protein synthesis was blocked. EFP-mediated degradation impaired the function of KLF5 in gene transcription. Although only unubiquitinated EFP interacted with KLF5, overexpression of EFP appeared to prevent the ubiquitination of KLF5, while resulting in heavy ubiquitination of the E3 itself. Furthermore, ubiquitination of EFP interrupted its interaction with KLF5. Although the mechanism for how EFP degrades KLF5 remains to be determined, the results of the present study suggest that oestrogen causes the degradation of KLF5 protein by inducing the expression of EFP in ER-positive breast cancer cells.
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