ArticleCancer science2022
DCAF13 promotes breast cancer cell proliferation by ubiquitin inhibiting PERP expression.
Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- The role of the WD40-repeat protein family in cancer.Molecular cancer · 2026Review
- Pro-tumourigenic effects of DCAF13 on the progression of colorectal cancer.Oncology letters · 2026Article
- Tissue-Specific Multi-Omics Integration Demonstrates Molecular Signatures Connecting Obesity to Immune Vulnerability.Metabolites · 2026Article
- Advances in protein ubiquitination modification and immune evasion of breast cancer.Frontiers in cell and developmental biology · 2026Review
- DCAF13 Regulates Cell Proliferation and Immune Escape of Hepatocellular Carcinoma Through Activating the NF-κB Pathway.Cell biochemistry and biophysics · 2025Article
- PERP suppresses breast cancer metastasis via the ATF3-HSPA6 signaling pathway.The Journal of international medical research · 2025Article
- N6-Methyladenosine Modification of PERP by RBM15 Enhances the Tumorigenesis of Lung Adenocarcinoma via p53 Signaling Pathway.Molecular biotechnology · 2025Article
- Targeting PERP promotes anti-tumor immunity in HNSCC by regulating tumor immune microenvironment and metabolic homeostasis.Molecular cancer · 2025Article
- GRB2 Promotes Malignant Behaviors of Breast Cancer by Modulating the Global Expression and Alternative Splicing Profiles in SK-BR-3 Cells Through Binding mRNA.Cancer medicine · 2025Article
- DCAF13 influences breast cancer chemotherapy resistance through metabolic reprogramming by regulating c-Myc expression.Medical oncology (Northwood, London, England) · 2025Article
- Intraductal chemotherapy for triple-negative breast cancer: a pathway to minimally invasive clinical treatment.BMC cancer · 2025Article
- Utilizing liquid-liquid biopolymer regulators to predict the prognosis and drug sensitivity of hepatocellular carcinoma.Biology direct · 2025Article
- The Clinical Prediction Value of the Ubiquitination Model Reflecting the Microenvironment Infiltration and Drug Sensitivity in Breast Cancer.Journal of Cancer · 2025Article
- Machine learning integration with multi-omics data constructs a robust prognostic model and identifies PTGES3 as a therapeutic target for precision oncology in lung adenocarcinoma.Frontiers in immunology · 2025Article
- DCAF13 promotes ovarian cancer progression by activating FRAS1-mediated FAK signaling pathway.Cellular and molecular life sciences : CMLS · 2024Article
- G-Quadruplex Forming DNA Sequence Context Is Enriched around Points of Somatic Mutations in a Subset of Multiple Myeloma Patients.International journal of molecular sciences · 2024Article
- DCAF13 inhibits the p53 signaling pathway by promoting p53 ubiquitination modification in lung adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2024Article
- Knockdown of LRP5 Promotes Proliferation and Invasion of Tongue Squamous Cell Carcinoma through Compensatory Activation of Akt Signaling.Journal of Cancer · 2024Article
- Function and prognosis analysis of nucleolus protein DCAF13 in breast cancer.Translational cancer research · 2023Article
- Integrated single-cell and bulk RNA sequencing analysis identifies a neoadjuvant chemotherapy-related gene signature for predicting survival and therapy in breast cancer.BMC medical genomics · 2023Article
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 2 countries.
Funding
Abstract
Evolutionarily conserved DDB1-and CUL4-associated factor 13 (DCAF13) is a recently discovered substrate receptor for the cullin RING-finger ubiquitin ligase 4 (CRL4) E3 ubiquitin ligase that regulates cell cycle progression. DCAF13 is overexpressed in many cancers, although its role in breast cancer is currently elusive. In this study we demonstrate that DCAF13 is overexpressed in human breast cancer and that its overexpression closely correlates with poor prognosis, suggesting that DCAF13 may serve as a diagnostic marker and therapeutic target. We knocked down DCAF13 in breast cancer cell lines using CRISPR/Cas9 and found that DCAF13 deletion markedly reduced breast cancer cell proliferation, clone formation, and migration both in vitro and in vivo. In addition, DCAF13 deletion promoted breast cancer cell apoptosis and senescence, and induced cell cycle arrest in the G1/S phase. Genome-wide RNAseq analysis and western blotting revealed that loss of DCAF13 resulted in both mRNA and protein accumulation of p53 apoptosis effector related to PMP22 (PERP). Knockdown of PERP partially reversed the hampered cell proliferation induced by DCAF13 knockdown. Co-immunoprecipitation assays revealed that DCAF13 and DNA damage-binding protein 1 (DDB1) directly interact with PERP. Overexpression of DDB1 significantly increased PERP polyubiquitination, suggesting that CRL4
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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.