ArticleJournal for immunotherapy of cancer2022
CUL3/SPOP complex prevents immune escape and enhances chemotherapy sensitivity of ovarian cancer cells through degradation of PD-L1 protein.
Article in Journal for immunotherapy of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Proanthocyanidins enhance antitumor immunity by promoting ubiquitin-proteasomal PD-L1 degradation via stabilization of LKB1 and SYVN1.The Journal of clinical investigation · 2026Article
- Paroxetine repurposing enhances antitumor immunity via SPOP-mediated PD-L1 ubiquitination and proteasomal degradation.Journal of experimental & clinical cancer research : CR · 2026Article
- DDIT3 drives nucleus pulposus cell PANoptosis and intervertebral disc degeneration progression.Apoptosis : an international journal on programmed cell death · 2026Article
- 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
- The role of E3 ligases and deubiquitinases in PD-L1 regulation and the tumor microenvironment in renal cell carcinoma.Medical oncology (Northwood, London, England) · 2025Review
- N6-methyladenosine modification of MEF2A weakens cetuximab sensitivity in colorectal cancer via PD-L1/SOX12 axis.Cell death discovery · 2025Article
- HKDC1 promotes ovarian cancer progression through boosting lipid metabolism and immune escape by stabilizing G6PC/G6PC2.Communications biology · 2025Article
- ZEB1 promotes the immune escape of ovarian cancer through the MCSF-CCL18 axis.Cancer cell international · 2025Article
- Post-translational modifications of immune checkpoints: unlocking new potentials in cancer immunotherapy.Experimental hematology & oncology · 2025Review
- Challenges and opportunities for the diverse substrates of SPOP E3 ubiquitin ligase in cancer.Theranostics · 2025Review
- Network Medicine-Based Strategy Identifies Maprotiline as a Repurposable Drug by Inhibiting PD-L1 Expression via Targeting SPOP in Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Knockdown of cullin 3 inhibits progressive phenotypes and increases chemosensitivity in cholangiocarcinoma cells.Molecular medicine reports · 2024Article
- Comprehensive analysis of the Cullin family of genes reveals that CUL7 and CUL9 are the significant prognostic biomarkers in colorectal cancer.American journal of translational research · 2024Article
- Recent advances in understanding the immune microenvironment in ovarian cancer.Frontiers in immunology · 2024Review
- Comprehensive analysis of integrin αvβ3/α6β1 in prognosis and immune escape of prostate cancer.Aging · 2023Article
- RIG-I promotes immune evasion of colon cancer by modulating PD-L1 ubiquitination.Journal for immunotherapy of cancer · 2023Article
- Current trends of high-risk gene Cul3 in neurodevelopmental disorders.Frontiers in psychiatry · 2023Review
- The E3 ubiquitin ligases regulate PD-1/PD-L1 protein levels in tumor microenvironment to improve immunotherapy.Frontiers in immunology · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCancer immune escape is a main obstacle in designing effective anticancer therapeutic approaches. Our work was aimed to explore the function of cullin 3 (CUL3) in ovarian cancer cell immune escape and chemosensitivity.
methodGain and loss of function assays were conducted to investigate the interactions among CUL3, speckle type POZ protein (SPOP) and programmed death ligand-1 (PD-L1) as well as their effects on ovarian cell malignant phenotypes and chemosensitivity. A mouse model of xenografted ovarian cells was further established for in vivo substantiation.
resultPoorly-expressed CUL3 and SPOP were found in ovarian cancer. Overexpression of CUL3 reduced malignant features as well as immune escape of ovarian cancer cells but enhanced chemosensitivity. Functionally, CUL3 degraded PD-L1 protein by forming complex with SPOP. Overexpression of CUL3 inhibited tumor formation and enhanced chemosensitivity of ovarian cancer cells in mice by degrading PD-L1 protein.
conclusionAll in all, CUL3/SPOP formed a complex to promote PD-L1 degradation to inhibit ovarian cancer cell immune escape and increase chemosensitivity, offering a therapeutic target for ovarian cancer treatment.
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