ArticleLaboratory investigation; a journal of technical methods and pathology2020
CCL8 secreted by tumor-associated macrophages promotes invasion and stemness of glioblastoma cells via ERK1/2 signaling.
Article in Laboratory investigation; a journal of technical methods and pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.
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Who cites it
122 citing papers in PubMed, 168 citations in OpenAlex.
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- GALNT6-glycosylated LRG1 mediates the interaction between M2 macrophages and pancreatic cancer cells by activating CCR1/PI3K/AKT axis.Molecular and cellular biochemistry · 2026Article
- The intersection of chemokine signaling with the hallmarks of cancer in glioblastoma.Journal of neuro-oncology · 2026Review
- 25 Years of Cancer Immunoediting: Dendritic Cells and Macrophages Filled the Missing Gap.Cancers · 2026Review
- KRAS inhibition is an effective therapy for appendiceal adenocarcinoma.Journal of hematology & oncology · 2026Article
- Integrative Transcriptomic Analysis Identifies Hypoxia-responsive Cell Cycle Hub Genes as Prognostic Markers in Glioblastoma.Annals of neurosciences · 2026Article
- Attract to kill: Exploring the potential of motility trapping as a novel treatment strategy for high-grade gliomas.Neuro-oncology · 2026Review
- Complement C5a/C5aR1 pathway facilitates glioblastoma progression via fostering glioma stem cell-macrophage symbiosis.Journal of neuroinflammation · 2026Article
- Role of NR2F2-mediated reprogramming of endothelial cells in glioblastoma progression.iScience · 2026Article
- PI3Kδ inhibition alters CD8 T cell differentiation and reprograms the tumor microenvironment following adoptive immunotherapy.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- KRAS inhibition is an effective therapy for appendiceal adenocarcinoma.bioRxiv : the preprint server for biology · 2026Article
- Phase II trial of hepatic arterial infusion chemotherapy plus bevacizumab and toripalimab for advanced biliary tract cancers: efficacy, safety, and exploratory analysis.Hepatobiliary surgery and nutrition · 2026Article
- Breast Cancer-Derived Extracellular Vesicle miR-425-5p (miR-425) Promotes Brain Metastasis via Activating Astrocytes Through the Novel miR-425-ZNF24-CCL8 Signaling Axis.International journal of molecular sciences · 2026Article
- Aberrant Activation of the Hedgehog Pathway in Cutaneous Melanoma: Therapeutic Potential of Pharmacological Inhibitors.International journal of molecular sciences · 2026Article
- Integrated transcriptomic and functional analyses reveal that NOX2 inhibition rewires the inflammatory landscape of macrophages.Frontiers in immunology · 2026Article
- Article
- ALKBH7 and NLRP3 Co-Expression: A Potential Prognostic and Immunometabolic Marker Set in Breast Cancer Subtypes.International journal of molecular sciences · 2025Article
- TREM2 facilitates gastric cancer progression and immune evasion via inhibiting TRIM21-mediated STAT1 degradation in tumor-associated macrophages.Cell death & disease · 2025Article
- Chimeric diphtheria toxin-CCL8 cytotoxic peptide for breast cancer management.Molecular oncology · 2025Article
62 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor-associated macrophages (TAMs) constitute a large population of glioblastoma and facilitate tumor growth and invasion of tumor cells, but the underlying mechanism remains undefined. In this study, we demonstrate that chemokine (C-C motif) ligand 8 (CCL8) is highly expressed by TAMs and contributes to pseudopodia formation by GBM cells. The presence of CCL8 in the glioma microenvironment promotes progression of tumor cells. Moreover, CCL8 induces invasion and stem-like traits of GBM cells, and CCR1 and CCR5 are the main receptors that mediate CCL8-induced biological behavior. Finally, CCL8 dramatically activates ERK1/2 phosphorylation in GBM cells, and blocking TAM-secreted CCL8 by neutralized antibody significantly decreases invasion of glioma cells. Taken together, our data reveal that CCL8 is a TAM-associated factor to mediate invasion and stemness of GBM, and targeting CCL8 may provide an insight strategy for GBM treatment.
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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.