ArticleCell death and differentiation2023
SPOP mutations promote tumor immune escape in endometrial cancer via the IRF1-PD-L1 axis.
Article in Cell death and differentiation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 48 citations in OpenAlex.
- Not only as a Cullin3 ligase adaptor, SPOP may also act as a molecular bridge.Genes & diseases · 2027Review
- IRF1-activated CA9 accelerates oral squamous cell carcinoma process via regulating cell glycolysis, migration, apoptosis and ferroptosis.Odontology · 2026Article
- Lactate-associated H3K18la upregulates RNF166 to promote immune evasion in hepatocellular carcinoma by remodeling c-Jun ubiquitination.Apoptosis : an international journal on programmed cell death · 2026Article
- Immune Spatial Organization Predicts Distant Metastasis Risk in Aggressive Localized Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Targeting E3 ubiquitin ligases: Mechanistic breakthroughs and novel clinical translation pathways for tumor radioimmunotherapy.Molecular cancer · 2026Review
- African swine fever virus pM448R protein promotes STUB1-mediated ubiquitin-proteasome degradation of IRF1 to attenuate type III interferon induction.Journal of virology · 2026Article
- High-throughput screening identifies a critical role of the SPOP-PABPC1 axis in lung adenocarcinoma progression.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Review
- SUMOylation in cancer: molecular mechanisms and therapeutic implications.Molecular cancer · 2026Review
- NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer.Cancer research · 2026Article
- Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Ubiquitin-centered post-translational modification crosstalk orchestrates tumor immunity and immunotherapy response.Experimental hematology & oncology · 2026Review
- Paroxetine repurposing enhances antitumor immunity via SPOP-mediated PD-L1 ubiquitination and proteasomal degradation.Journal of experimental & clinical cancer research : CR · 2026Article
- IRF1 suppresses gastric tumorigenesis via dual PI3K/AKT-ERK pathway modulation and functional antagonism of oncogenic MX2.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Baicalin attenuates the immune escape of oral squamous cell carcinoma by reducing lactate accumulation in tumor microenvironment.Journal of advanced research · 2025Article
- PD-1/PD-L1 Cancer Immunotherapeutics Reshape Tumor Microenvironment - Clinical Evidence and Molecular Mechanisms for AI-based Precision Medicine.Clinical reviews in allergy & immunology · 2025Review
- Exploration of propionate metabolism-related genes to predict prognosis and immunotherapy response in ovarian cancer.Journal of ovarian research · 2025Article
- Hepatic NMNAT1 is required to defend against alcohol-associated fatty liver disease.Science advances · 2025Article
- LMNB2-mediated high PD-L1 transcription triggers the immune escape of hepatocellular carcinoma.Cell death discovery · 2025Article
- SPOP/NOLC1/B4GALT1 signaling axis enhances paclitaxel resistance in endometrial cancer by inducing O-dysglycosylation.Oncogene · 2025Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Blockade of programmed cell death 1 (PD-1)/programmed cell death 1 ligand (PD-L1) has evolved into one of the most promising immunotherapy strategies for cancer patients. Tumor cells frequently overexpress PD-L1 to evade T cell-mediated immune surveillance. However, the specific genetic alterations that drive aberrant overexpression of PD-L1 in cancer cells remain poorly understood. The gene encoding the E3 ubiquitin ligase substrate-binding adaptor SPOP is frequently mutated in endometrial cancer (EC). Here, we report that SPOP negatively regulates PD-L1 expression at the transcriptional level. Wild-type SPOP binds to IRF1, a primary transcription factor responsible for the inducible expression of PD-L1, and subsequently triggers its ubiquitin- proteasomal degradation to suppress IRF1-mediated transcriptional upregulation of PD-L1. In contrast, EC-associated SPOP mutants lose their capacity to degrade IRF1 but stabilize IRF1, and upregulate PD-L1 expression. EC-associated SPOP mutations accelerate xenograft tumor growth partially by increasing IRF1 and PD-L1 expression. Together, we identify SPOP as a negative regulator of the IRF1-PD-L1 axis and characterize the critical roles of IRF1 and PD-L1 in SPOP mutation-driven tumor immune evasion in EC.
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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.