ArticleNature communications2015
BAP1 promotes breast cancer cell proliferation and metastasis by deubiquitinating KLF5.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.
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Who cites it
136 citing papers in PubMed, 207 citations in OpenAlex.
- HMGB1 directly activates BAP1 transcription to sustain tumor growth in mesothelioma.Cell death and differentiation · 2026Article
- Bap1-mediated deubiquitination determines immune tolerance and anti-tumor immunity via modulating eTreg cell differentiation and ferroptosis.Cell death and differentiation · 2026Article
- Epigenetic regulation of ACSL4 via H2A monoubiquitylation connects lipid metabolism to BAP1-mediated ferroptosis.Cell death and differentiation · 2026Article
- CDK6/4 inactivates BAP1 deubiquitinase destabilizing VHL to promote metastatic colonization in liver.Molecular cancer · 2026Article
- White-to-brown adipose switching promotes bladder cancer progression.Neoplasia (New York, N.Y.) · 2026Article
- AMPK-activated BAP1 regulates pVHL stability and tumor-suppressive functions.Cell death and differentiation · 2026Article
- Tumor suppressor BAP1 emerges as a key regulator of metabolism and cell death in tumors.Frontiers in cell and developmental biology · 2026Review
- Isoliquiritigenin Impedes Breast Cancer Progression through PITX1-PFKP-Mediated Glycolysis Reprogramming.Oncology research · 2026Article
- Molecular Subtypes of Mixed Gastric Cancer Defined by Machine Learning for Predicting Prognosis and Treatment Response.Current medicinal chemistry · 2026Article
- Interplay between Epigenetic and Transcription Factors Mediating Drug Resistance via Stem Cells in Breast Cancer.ACS omega · 2025Review
- PR inhibition stimulates G6PD expression to enhance malignancy in luminal breast cancer.Cell death & disease · 2025Article
- USP44 promotes chemotherapeutic drug resistance of triple negative breast cancer through EZH2 protein stability.Cancer biology & therapy · 2025Article
- Molecular regulation by ubiquitin-specific proteases (USPs) in HCC: cell cycle, oncogenic signaling, and beyond.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Characterization of BRCA1-Associated Protein-1 (BAP1) Aggregation Properties Induced by Cancer-Associated Mutations.Chembiochem : a European journal of chemical biology · 2025Article
- Restoration of BAP1 activity via base editing suppresses anchorage-independent survival in kidney cancer.Cancer cell international · 2025Article
- Research progress of DUB enzyme in breast cancer.Clinical and experimental medicine · 2025Review
- A novel SWI/SNF complex promotes triple-negative breast cancer progression.Cellular & molecular biology letters · 2025Article
- UFMylation maintains tumor suppressor pVHL stability by activating the deubiquitinase BAP1.Science advances · 2025Article
- NAT10 Promotes Gastric Cancer Liver Metastasis by Modulation of M2 Macrophage Polarization and Metastatic Tumor Cell Hepatic Adhesion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Positive Feedback Regulation between KLF5 and XPO1 Promotes Cell Cycle Progression of Basal like Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
76 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor KLF5 is highly expressed in basal-like breast cancer and promotes breast cancer cell proliferation, survival, migration and tumour growth. Here we show that, in breast cancer cells, KLF5 is stabilized by the deubiquitinase (DUB) BAP1. With a genome-wide siRNA library screen of DUBs, we identify BAP1 as a bona fide KLF5 DUB. BAP1 interacts directly with KLF5 and stabilizes KLF5 via deubiquitination. KLF5 is in the BAP1/HCF-1 complex, and this newly identified complex promotes cell cycle progression partially by inhibiting p27 gene expression. Furthermore, BAP1 knockdown inhibits tumorigenicity and lung metastasis, which can be rescued partially by ectopic expression of KLF5. Collectively, our findings not only identify BAP1 as the DUB for KLF5, but also reveal a critical mechanism that regulates KLF5 expression in breast cancer. Our findings indicate that BAP1 could be a potential therapeutic target for breast and other cancers.
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