ArticleInternational journal of biological sciences2022
Histone Deacetylase Inhibitors (HDACi) Promote KLF5 Ubiquitination and Degradation in Basal-like Breast Cancer.
Article in International journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- Hypophosphatemia as a Potential Class Effect of Histone Deacetylase Inhibitors: Evidence from Disproportionality Analysis and Mendelian Randomization Analysis of Drug Targets.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Cancer and aging: complex associations and therapeutic targets.Molecular biomedicine · 2026Review
- Dual-dimensional profiling of host genomic variations and HPV integration in PD-L1-stratified cervical cancer via Oxford Nanopore Technology.Journal of translational medicine · 2026Article
- Epigenetic regulation in cancer chemoresistance and combined therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- Ubiquitination in cancer: mechanisms and therapeutic opportunities.Cancer communications (London, England) · 2025Review
- Acetylation: a new target for protein degradation in cancer.Trends in cancer · 2025Review
- LN-439A, a novel BAP1 inhibitor, suppresses the growth of basal-like breast cancer by degrading KLF5.Acta pharmacologica Sinica · 2025Article
- KLF5 inhibition initiates epithelial-mesenchymal transition in non-transformed human squamous epithelial cells.Biochimica et biophysica acta. Molecular cell research · 2024Article
- Elevated choline drives KLF5-dominated transcriptional reprogramming to facilitate liver cancer progression.Oncogene · 2024Article
- Advances in targeting histone deacetylase for treatment of solid tumors.Journal of hematology & oncology · 2024Review
- Prospects for breast cancer immunotherapy using microRNAs and transposable elements as objects.Exploration of targeted anti-tumor therapy · 2024Review
- Current treatment strategies targeting histone deacetylase inhibitors in acute lymphocytic leukemia: a systematic review.Frontiers in oncology · 2024Review
- Upregulated PARP1 confers breast cancer resistance to CDK4/6 inhibitors via YB-1 phosphorylation.Experimental hematology & oncology · 2023Article
- KLF5 Promotes Tumor Progression and Parp Inhibitor Resistance in Ovarian Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- KLF5 inhibition potentiates anti-PD1 efficacy by enhancing CD8Theranostics · 2023Article
- Protein acylation: mechanisms, biological functions and therapeutic targets.Signal transduction and targeted therapy · 2022Review
- Review
- Pre-pubertal oocytes harbor altered histone modifications and chromatin configuration.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Basal-like breast cancer (BLBC) accounts for approximately 15% of all breast cancer cases, and patients with BLBC have a low survival rate. Our previous study demonstrated that the KLF5 transcription factor promotes BLBC cell proliferation and tumor growth. In this study, we demonstrated that the histone deacetylase inhibitors (HDACi), suberoylanilide hydroxamic acid (SAHA), and trichostatin A (TSA), increased KLF5 acetylation at lysine 369 (K369), downregulated KLF5 protein expression levels, and decreased cell viability in BLBC cell lines. HDACi target KLF5 for proteasomal degradation by promoting KLF5 protein ubiquitination. K369 acetylation of KLF5 decreases the binding between KLF5 and its deubiquitinase, BAP1. These findings revealed a novel mechanism by which HDACi suppress BLBC, and a novel crosstalk between KLF5 protein acetylation and ubiquitination.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.