ArticleBiochemical and biophysical research communications2018
HDAC-mediated deacetylation of KLF5 associates with its proteasomal degradation.
Article in Biochemical and biophysical research communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Unbiased screening identifies regulators of cell-cell adhesion and treatment options in pemphigus.Nature communications · 2024Article
- Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024Review
- Therapeutic potential of natural antisense transcripts and various mechanisms involved for clinical applications and disease prevention.RNA biology · 2024Review
- KLF5 and p53 comprise an incoherent feed-forward loop directing cell-fate decisions following stress.Cell death & disease · 2023Article
- New insights into KLFs and SOXs in cancer pathogenesis, stemness, and therapy.Seminars in cancer biology · 2023Review
- KLF5 inhibition potentiates anti-PD1 efficacy by enhancing CD8Theranostics · 2023Article
- Histone Deacetylase Inhibitors (HDACi) Promote KLF5 Ubiquitination and Degradation in Basal-like Breast Cancer.International journal of biological sciences · 2022Article
- The roles and regulation of the KLF5 transcription factor in cancers.Cancer science · 2021Review
- Acetylation of KLF5 maintains EMT and tumorigenicity to cause chemoresistant bone metastasis in prostate cancer.Nature communications · 2021Article
- The Partial Role of KLF4 and KLF5 in Gastrointestinal Tumors.Gastroenterology research and practice · 2021Review
- TGF-β causes Docetaxel resistance in Prostate Cancer via the induction of Bcl-2 by acetylated KLF5 and Protein Stabilization.Theranostics · 2020Article
- ZNF326 promotes malignant phenotype of glioma by up-regulating HDAC7 expression and activating Wnt pathway.Journal of experimental & clinical cancer research : CR · 2019Article
- EZH2 Regulates Protein Stability via Recruiting USP7 to Mediate Neuronal Gene Expression in Cancer Cells.Frontiers in genetics · 2019Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Krüppel-like factor 5 (KLF5) is a basic transcription factor that regulates diverse cellular processes during tumor development. Acetylation of KLF5 at lysine 369 (K369) reverses its function from promoting to suppressing cell proliferation and tumor growth. In this study, we examined the regulation of KLF5 by histone deacetylases in the prostate cancer cell line DU 145. While confirming the functions of HDAC1/2 in KLF5 deacetylation and the promotion of cell proliferation, we found that the knockdown of HDAC1/2 upregulated KLF5 protein but not KLF5 mRNA, and the increase in KLF5 protein level by silencing HDAC1/2 was at least in part due to decreased proteasomal degradation. Deacetylase activity was required for HDAC1/2-mediated KLF5 degradation, and mutation of KLF5 to an acetylation-mimicking form prevented its degradation, even though the mutation did not affect the binding of KLF5 with HDAC1/2. Mutation of K369 to arginine, which prevents acetylation, did not affect the binding of KLF5 to HDAC1 or the response of KLF5 to HDAC1/2-promoted degradation. These findings provide a novel mechanistic association between the acetylation status of KLF5 and its protein stability. They also suggest that maintaining KLF5 in a deacetylated form may be an important mechanism by which KLF5 and HDACs promote cell proliferation and tumor growth.
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