Excel · study · 2026
CD300A drives glioblastoma progression by orchestrating M2 macrophage polarization via the JAK2/STAT3 signaling axis
Listed in NCBI GEO
Glioblastoma (GBM) is the most lethal primary intracranial malignancy, characterized by aggressive recurrence and a dismal prognosis.
Description
Despite the implementation of multimodal standard-of-care therapies, including maximal surgical resection, radiotherapy, and chemotherapy, clinical outcomes remain unsatisfactory. A critical determinant of therapeutic resistance is the highly immunosuppressive tumor microenvironment (TME).
Tumor-associated macrophages (TAMs), which constitute 30-50% of the tumor mass, are the predominant immune population within the TME and key orchestrators of GBM-associated immunosuppression. While TAMs predominantly acquire a protumoral M2-like phenotype to facilitate tumor progression via the secretion of cytokines, angiogenic factors, and matrix metalloproteinases, the molecular mechanisms governing this polarization remain elusive.
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Herein, we identify the immunoregulatory receptor CD300A as a critical driver of M2 macrophage polarization in GBM. Analysis of clinical specimens demonstrated that CD300A is significantly upregulated in GBM tissues and positively correlates with the M2 marker CD163. In a macrophage model, we found that upon M2 induction, CD300A expression was markedly upregulated, paralleling the induction of canonical M2 markers, including CD206 and Arg-1.
Functionally, ectopic overexpression of CD300A markedly upregulated canonical M2 markers CD206, Arg-1, and FIZZ1, whereas CD300A knockdown attenuated this phenotype. Mechanistically, we demonstrate that CD300A promotes M2 polarization by activating the JAK2/STAT3 signaling axis. Furthermore, CD300A-mediated M2 polarization was found to enhance the proliferation, migration, and invasion of GBM cells via the induction of VEGFA secretion.
Collectively, our findings delineate a novel CD300A-JAK2/STAT3-VEGFA signaling axis that couples immune modulation with malignant progression, highlighting CD300A as a potential therapeutic target for modulating TAMs in GBM.
Links
Get the data
- GEO FTP directory ftp.ncbi.nlm.nih.gov/geo/series/GSE337nnn/GSE337492 ↗
download · from NCBI GEO
Where it is published
- GEO accession page ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE337492 ↗
landing page · from NCBI GEO
Documentation and papers
- PRJNA1489526 ncbi.nlm.nih.gov/bioproject/PRJNA1489526 ↗
project · from NCBI GEO
Topics
- Stated by source
- Expression profiling by high throughput sequencing · Homo sapiens
- From keywords
- Life Sciences
- Inferred from text
- Cancer 65%
Provenance · 1 source records, 8 field assertions
| Source | Key | Last seen | Raw |
|---|---|---|---|
| NCBI GEO | GSE337492 | 14 d ago | JSON v1 |
| Field | Assertion | Extractor | Evidence |
|---|---|---|---|
| access_level | source · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| concepts[disease].local:disease:cancer | enrichment · NCBI GEO | keyword-concept-rules@1.0.0 | title+description (65%) |
| concepts[field].local:field:life-sciences | mapping · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| concepts[method].geo_series_type:expression-profiling-by-high-throughput-sequencing | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /gdstype |
| concepts[organism].NCBITaxon:9606 | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /taxon |
| description | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /summary |
| publication_date | source · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| title | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /title |