ArticleJournal of experimental & clinical cancer research : CR2020
SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway.
Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 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.
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Who cites it
18 citing papers in PubMed, 19 citations in OpenAlex.
- Retraction Note: BRD9 inhibition promotes PUMA-dependent apoptosis and augments the effect of imatinib in gastrointestinal stromal tumors.Cell death & disease · 2025Article
- Retraction Note: The miR-30a-5p/CLCF1 axis regulates sorafenib resistance and aerobic glycolysis in hepatocellular carcinoma.Cell death & disease · 2025Article
- Targeting the Tumor Epigenetic Regulator SETDB1 for Tumor Therapy.Current cancer drug targets · 2025Review
- Epigenetic tuning of tumour-associated macrophages (TAMs): a potential approach in hepatocellular carcinoma (HCC) immunotherapy.Expert reviews in molecular medicine · 2024Review
- Retraction Note: The BET inhibitor I-BET762 inhibits pancreatic ductal adenocarcinoma cell proliferation and enhances the therapeutic effect of gemcitabine.Scientific reports · 2023Article
- Gene-Smoking Interaction Analysis for the Identification of Novel Asthma-Associated Genetic Factors.International journal of molecular sciences · 2023Article
- RNA-binding protein DHX9 promotes glioma growth and tumor-associated macrophages infiltration via TCF12.CNS neuroscience & therapeutics · 2023Article
- C5aR1 promotes the progression of colorectal cancer by EMT and activating Wnt/β-catenin pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- Article
- Mechanism and therapeutic potential of tumor-immune symbiosis in glioblastoma.Trends in cancer · 2022Review
- METTL7B contributes to the malignant progression of glioblastoma by inhibiting EGR1 expression.Metabolic brain disease · 2022Article
- Increased Expression of SETDB1 Predicts Poor Prognosis in Multiple Myeloma.BioMed research international · 2022Article
- Targeting tumor-associated macrophages for the immunotherapy of glioblastoma: Navigating the clinical and translational landscape.Frontiers in immunology · 2022Review
- Signal Pathways Involved in the Interaction Between Tumor-Associated Macrophages/TAMs and Glioblastoma Cells.Frontiers in oncology · 2022Review
- Macrophages/Microglia in the Glioblastoma Tumor Microenvironment.International journal of molecular sciences · 2021Review
- Potential therapeutic targets in the tumor microenvironment of hepatocellular carcinoma: reversing the protumor effect of tumor-associated macrophages.Journal of experimental & clinical cancer research : CR · 2021Review
- SETDB1 in cancer: overexpression and its therapeutic implications.American journal of cancer research · 2021Review
- Insight into the multi-faceted role of the SUV family of H3K9 methyltransferases in carcinogenesis and cancer progression.Biochimica et biophysica acta. Reviews on cancer · 2021Review
Corrections and comments
- Retraction · 2022-09-21Concerns/Issues about Image · Lack of IRB/IACUC Approval and/or Compliance · Original Data and/or Images not Provided and/or not Available ·
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastoma is a common disease of the central nervous system (CNS), with high morbidity and mortality. In the infiltrate in the tumor microenvironment, tumor-associated macrophages (TAMs) are abundant, which are important factors in glioblastoma progression. However, the exact details of TAMs in glioblastoma progression have yet to be determined.
methodsThe clinical relevance of SET domain bifurcated 1 (SETDB1) was analyzed by immunohistochemistry, real-time PCR and Western blotting of glioblastoma tissues. SETDB1-induced cell proliferation, migration and invasion were investigated by CCK-8 assay, colony formation assay, wound healing and Transwell assay. The relationship between SETDB1 and colony stimulating factor 1 (CSF-1), as well as TAMs recruitment was examined by Western blotting, real-time PCR and syngeneic mouse model.
resultsOur findings showed that SETDB1 upregulated in glioblastoma and relative to poor progression. Gain and loss of function approaches showed the SETDB1 overexpression promotes cell proliferation, migration and invasion in glioblastoma cells. However, knockdown SETDB1 exerted opposite effects in vitro. Moreover, SETDB1 promotes AKT/mTOR-dependent CSF-1 induction and secretion, which leads to macrophage recruitment in the tumor, resulted in tumor growth.
conclusionOur research clarified that SETDB1 regulates of tumor microenvironment and hence presents a potential therapeutic target for treating glioblastoma.
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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.