ArticleCancer cell international2023
The MYBL2-CCL2 axis promotes tumor progression and resistance to anti-PD-1 therapy in ovarian cancer by inducing immunosuppressive macrophages.
Article in Cancer cell international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- MYBL2 promotes malignant phenotypes and M2-like macrophage polarization through CCL2 in non-small cell lung cancer.Molecular and cellular biochemistry · 2026Article
- STAT3 Inhibitor Suppresses CCL2-dependent Recruitment and M2 Polarization of Tumor-associated Macrophages to Enhance Antitumor Immunity in Ovarian Cancer.Applied biochemistry and biotechnology · 2026Article
- FBXW7 Inhibited M2 Macrophage Polarization in Endometrial Cancer by Reducing CCL2 Secretion Through Ubiquitination of MYBL2 Subtitle: The Role of FBXW7 on M2 Macrophage Polarization in EC.Biochemical genetics · 2026Article
- FGFR Inhibitor AZD4547 Disrupts Inflammatory CAF Crosstalk With Cancer Cells and Macrophages and Attenuates Metastasis in Pancreatic Cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Viral rewiring of DDR signaling activates a pro-survival network that drives chemotherapy resistance.bioRxiv : the preprint server for biology · 2026Article
- Correlated expression of MYBL2 and CCL5 defines an immunosuppressive microenvironment and predicts poor prognosis in intrahepatic cholangiocarcinoma.BMC cancer · 2026Article
- TAMs in the Gynecological Tumor Microenvironment: Insights from Cross-Cancer Studies for Immunotherapy.Cancers · 2026Review
- A Pan-Cancer Transcriptomic Signature for Conserved Molecular Programs Underlying Premalignant-Malignant Progression Across Common Carcinomas.Dentistry journal · 2026Article
- LDRT combined with anti-PD-1 promotes tumor regression in head and neck squamous cell carcinoma through tumor metaprogram evolution and immune cell reprogramming.Journal of experimental & clinical cancer research : CR · 2026Article
- High expression of formin-2 can promote ovarian cancer chemoresistance via immunosuppressive macrophages.Functional & integrative genomics · 2025Article
- Bioinformatic Approach to Identify PotentialInternational journal of molecular sciences · 2025Article
- TRIM32 promotes tumor immune evasion and impedes Anti-PD-1 treatment by inducing immunosuppressive macrophages in gastric cancer.Journal of translational medicine · 2025Article
- Article
- A single-cell network approach to decode metabolic regulation in gynecologic and breast cancers.NPJ systems biology and applications · 2025Article
- System Analysis Identifies MYBL2 As a Novel Oncogene Target for Metastatic Prostate Cancer.Journal of Cancer · 2025Article
- Article
- Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Unveiling the contribution of tumor-associated macrophages in driving epithelial-mesenchymal transition: a review of mechanisms and therapeutic Strategies.Frontiers in pharmacology · 2024Review
- Integrated machine learning identifies a cellular senescence-related prognostic model to improve outcomes in uterine corpus endometrial carcinoma.Frontiers in immunology · 2024Article
- Single-cell RNA sequencing reveals that MYBL2 in malignant epithelial cells is involved in the development and progression of ovarian cancer.Frontiers in immunology · 2024Article
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundAn immunosuppressive tumor microenvironment in ovarian cancer facilitates tumor progression and resistance to immunotherapy. The function of MYB Proto-Oncogene Like 2 (MYBL2) in the tumor microenvironment remains largely unexplored.
methodsA syngeneic intraovarian mouse model, flow cytometry analysis, and immunohistochemistry were used to explore the biological function of MYBL2 in tumor progression and immune escape. Molecular and biochemical strategies-namely RNA-sequencing, western blotting, quantitative reverse transcription-polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assay, multiplex immunofluorescence, chromatic immunoprecipitation assay (CHIP) and luciferase assay-were used to reveal the mechanisms of MYBL2 in the OVC microenvironment.
resultsWe found tumor derived MYBL2 indicated poor prognosis and selectively correlated with tumor associated macrophages (TAMs) in ovarian cancer. Mechanically, C-C motif chemokine ligand 2 (CCL2) transcriptionally activated by MYBL2 induced TAMs recruitment and M2-like polarization in vitro. Using a syngeneic intraovarian mouse model, we identified MYBL2 promoted tumor malignancyand increased tumor-infiltrating immunosuppressive macrophages. Cyclin-dependent kinase 2 (CDK2) was a known upstream kinase to phosphorylate MYBL2 and promote its transcriptional function. The upstream inhibitor of CDK2, CVT-313, reprogrammed the tumor microenvironment and reduced anti-PD-1 resistance.
conclusionsThe MYBL2/CCL2 axis contributing to TAMs recruitment and M2-like polarization is crucial to immune evasion and anti-PD-1 resistance in ovarian cancer, which is a potential target to enhance the efficacy of immunotherapy.
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