ArticleDiscover oncology2025
BRD8 inhibits colorectal cancer progression through TGF-β1-mediated tumor-associated macrophage recruitment.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Recent Progress and Prospect in Studying Selective Inhibitors Toward Bromodomain Family Members.Molecules (Basel, Switzerland) · 2026Review
- Progranulin promotes glioma progression through the M2-TGF-β axis: targeted therapy with SORT1-loaded HAMA hydrogel microspheres.American journal of translational research · 2026Article
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Authors and funding
4 authors.
Funding
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Abstract
Colorectal cancer (CRC) ranks as one of the most malignant solid tumors worldwide. Bromodomain containing 8 (BRD8) functions as an oncogene in various cancers. This study aimed to investigate the roles of BRD8 in CRC. mRNA expression was detected using reverse transcription-quantitative PCR (RT-qPCR). Protein expression was detected using Western blot. The expression of macrophage markers was detected using immunohistochemistry and immunofluorescence. Cell viability was detected using Cell Counting Kit-8 (CCK-8) assay. Macrophage function was detected using flow cytometry. Cell migration and invasion was detected using transwell assays. We found that high levels of BRD8 mediated the predominance of M2-like tumor-associated macrophages (TAM2) and predicted poor prognosis of CRC patients. However, BRD8 knockdown suppressed TAM2 polarization as well as the migration and invasion of CRC cells. Mechanically, BRD8-mediated the upregulation of transforming growth factor β1 (TGF-β1), overexpression of which promoted TAM2 polarization and aggressiveness of CRC cells. Taken together, BRD8 deficiency suppressed TAM2 polarization, inhibiting the progression of CRC. Therefore, BRD8 may be a therapeutic target for CRC.
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