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BRD8 inhibits colorectal cancer progression through TGF-β1-mediated tumor-associated macrophage recruitment
Liang Xu1, Yejia Mo2, Bingqi Yu3
1General Surgery Department, Zhejiang Hospital, No.1229 Gudun Road, Xihu, Hangzhou, 310013, Zhejiang, China.
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.
Insights
Bromodomain containing 8 (BRD8) promotes colorectal cancer (CRC) by increasing M2-like tumor-associated macrophages (TAM2). BRD8 deficiency inhibits CRC progression and TAM2 polarization, suggesting BRD8 as a potential therapeutic target.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Colorectal cancer (CRC) is a leading cause of cancer mortality globally.
- Bromodomain containing 8 (BRD8) is implicated as an oncogene in several cancer types.
- The specific role of BRD8 in CRC pathogenesis remains to be fully elucidated.
Purpose of the Study:
- To investigate the role of BRD8 in colorectal cancer.
- To explore the relationship between BRD8 expression and tumor-associated macrophages (TAMs) in CRC.
- To determine the underlying mechanisms by which BRD8 influences CRC progression.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) and Western blotting for gene and protein expression analysis.
- Immunohistochemistry and immunofluorescence for macrophage marker detection.
- Cell Counting Kit-8 (CCK-8), flow cytometry, and Transwell assays to assess cell viability, macrophage function, migration, and invasion.
Main Results:
- High BRD8 expression correlated with M2-like TAMs (TAM2) predominance and poor CRC patient prognosis.
- BRD8 knockdown suppressed TAM2 polarization and reduced CRC cell migration and invasion.
- BRD8 upregulated transforming growth factor β1 (TGF-β1), which promoted TAM2 polarization and CRC cell aggressiveness.
Conclusions:
- BRD8 deficiency suppresses TAM2 polarization, thereby inhibiting colorectal cancer progression.
- BRD8 plays a significant role in promoting CRC aggressiveness through TAM2 modulation.
- BRD8 represents a potential therapeutic target for colorectal cancer treatment.
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