ArticleMolecular oncology2022
Deubiquitination of FBP1 by USP7 blocks FBP1-DNMT1 interaction and decreases the sensitivity of pancreatic cancer cells to PARP inhibitors.
Article in Molecular oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- ZUP1 promotes DNA repair and immune evasion to drive olaparib resistance in triple-negative breast cancer.Journal of advanced research · 2026Article
- Metabolic Regulation of Immune Responses: Molecular Mechanisms, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Emerging roles of USP7 in tumor immune evasion, metabolic reprogramming, and therapeutic resistance.Frontiers in immunology · 2026Review
- Post-Translational Modifications: Key "Regulators" of Pancreatic Cancer Malignant Phenotype-Advances in Mechanisms and Targeted Therapies.Biomedicines · 2025Review
- Extracellular vesicles-delivered circDB promotes ischemic muscle repair through the miR-34a/USP7/Notch1 signaling pathway.Regenerative therapy · 2025Article
- The multifaceted roles of deubiquitinating enzymes (DUBs) in pancreatic ductal adenocarcinoma.Cell death & disease · 2025Review
- AKT and DUBs: a bidirectional relationship.Cellular & molecular biology letters · 2025Review
- MLN4924 suppresses tumor metabolism and growth of clear cell renal cell carcinoma by stabilizing nuclear FBP1.Cell death discovery · 2025Article
- O-GlcNAcylation of FBP1 promotes pancreatic cancer progression by facilitating its Lys48-linked polyubiquitination in hypoxic environments.Oncogenesis · 2025Article
- The role of fructose-1,6-bisphosphatase 1 on regulating the cancer progression and drug resistance.Discover oncology · 2025Review
- Involvement of the ubiquitin-proteasome system in the regulation of the tumor microenvironment and progression.Genes & diseases · 2025Review
- Lysine acetylation and its role in the pathophysiology of acute pancreatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Ubiquitin-specific protease 7 maintains c-Myc stability to support pancreatic cancer glycolysis and tumor growth.Journal of translational medicine · 2024Article
- Ubiquitination and deubiquitination in cancer: from mechanisms to novel therapeutic approaches.Molecular cancer · 2024Review
- Drug resistance mechanisms and treatment strategies mediated by Ubiquitin-Specific Proteases (USPs) in cancers: new directions and therapeutic options.Molecular cancer · 2024Review
- Ubiquitination-specific protease 7 enhances stemness of hepatocellular carcinoma by stabilizing basic transcription factor 3.Functional & integrative genomics · 2024Article
- Review
- Ubiquitin signaling in pancreatic ductal adenocarcinoma.Frontiers in molecular biosciences · 2023Review
- Highlights in USP7 inhibitors for cancer treatment.Frontiers in chemistry · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poly[ADP-ribose] polymerase (PARP) inhibitors can block DNA single-strand damage repair and subsequently increase double-stranded breaks (DSBs) by reducing the activity of the PARP1 protease and by preventing the PARP1 protein from dissociating from chromatin. Tumors with the BRCA mutation are particularly sensitive to PARP inhibitors. So far, PARP inhibitors (Olaparib) have been used to treat pancreatic cancer patients with BRCA mutation. However, these patients are prone to PARP inhibitor resistance. Our previous studies suggest that fructose-1,6-bisphosphatase 1 (FBP1) is responsible for the sensitivity to various anticancer agents, such as gemcitabine or mitogen-activated protein kinase kinase (MEK) inhibitors. In this study, we demonstrate that FBP1 regulates the sensitivity to PARP inhibitors in pancreatic cancer. Then, we showed that nuclear FBP1 is responsible for this process by interacting with DNA (cytosine-5)-methyltransferase 1 (DNMT1) and trapping PARP1 in chromatin. Moreover, we revealed that ubiquitin carboxyl-terminal hydrolase 7 (USP7) binds to and induces the deubiquitination of FBP1, which prevented FBP1 from translocating to the nucleus. Finally, we demonstrated that USP7 inhibitors enhanced the antitumor effect of PARP inhibitors in an FBP1-dependent manner. Collectively, our results identify a novel USP7-FBP1-DNMT1 signaling axis in pancreatic cancer, which might indicate that USP7 inhibitors and PARP inhibitors might have more powerful antitumor effects than PARP inhibitors alone in pancreatic cancer patients.
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