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Updated: Sep 4, 2025
In Vitro Assay to Study Tumor-macrophage Interaction
Published on: August 1, 2019
Mapping the Tumor Microenvironment in TNBC and Deep Exploration for M1 Macrophages-Associated Prognostic Genes
Baojin Xu1,2,3, Hefen Sun1,2, Xiaoqing Song1,2
1Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, China.
Abstract:
Triple negative breast cancer (TNBC) remains the worst molecular subtype due to high heterogeneity and lack of effective therapeutic targets. Here we investigated the tumor and immune microenvironment heterogeneity of TNBC using scRNA-seq and bulk RNA-seq data from public databases and our cohort. Macrophage subpopulations accounted for a high proportion of tumor immune microenvironment (TIME), and M1 macrophages were associated with better clinical outcomes. Furthermore, three maker genes including IFI35, PSMB9, and SAMD9L showed a close connection with M1 macrophages. Specifically, IFI35 was positively associated with macrophage activation, chemotaxis, and migration. Also, patients with high IFI35 expression had a better prognosis. In vitro studies subsequently demonstrated that IFI35 was upregulated during the M1 subtype differentiation of macrophages. In summary, our data suggested that IFI35 maybe a promising novel target that helps to reshape macrophage polarization towards the M1 subtype for anti-tumor effects.
Insights
Triple negative breast cancer (TNBC) is aggressive due to its heterogeneity. Targeting IFI35 may enhance M1 macrophage polarization for better anti-tumor effects in TNBC.
Area of Science:
- Oncology
- Immunology
- Genetics
Background:
- Triple negative breast cancer (TNBC) is the most aggressive subtype with limited therapeutic options.
- Tumor heterogeneity and immune microenvironment complexity contribute to TNBC's poor prognosis.
Purpose of the Study:
- To investigate the tumor and immune microenvironment heterogeneity in TNBC.
- To identify potential therapeutic targets for improving TNBC treatment outcomes.
Main Methods:
- Utilized single-cell RNA sequencing (scRNA-seq) and bulk RNA sequencing (bulk RNA-seq) data.
- Analyzed public databases and a patient cohort to assess tumor microenvironment characteristics.
- Conducted in vitro studies to validate gene function in macrophage differentiation.
Main Results:
- Macrophage subpopulations, particularly M1 macrophages, were crucial components of the tumor immune microenvironment (TIME).
- M1 macrophages correlated with improved clinical outcomes in TNBC patients.
- IFI35, PSMB9, and SAMD9L were identified as key maker genes associated with M1 macrophages.
- IFI35 expression was linked to macrophage activation, migration, and better patient prognosis.
- In vitro studies confirmed IFI35 upregulation during M1 macrophage differentiation.
Conclusions:
- IFI35 plays a significant role in macrophage polarization towards the M1 subtype.
- IFI35 represents a promising therapeutic target for reprogramming the tumor immune microenvironment in TNBC.
- Targeting IFI35 could enhance anti-tumor immunity and improve clinical outcomes for TNBC patients.
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