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Updated: Mar 18, 2026
Macrophage Differentiation and Polarization into an M2-Like Phenotype using a Human Monocyte-Like THP-1 Leukemia Cell Line
Published on: August 2, 2021
SLAMF8 Promotes M2 Polarization of Macrophages and Enhances Breast Cancer Proliferation
Jilin Kong1, Rui Tian1, Shuyan Li1
1Department of Breast Surgery, Yantaishan Hospital, Yantai, Shandong, 264003, People's Republic of China.
Background:
Breast cancer is characterized by a complex pathogenesis and diverse clinical manifestations. Tumor-associated macrophages (TAMs) play a pivotal role in tumorigenesis, metastasis, and response to anticancer therapies. This study aimed to analyze the functional role of signaling lymphocytic activation molecule family 8 (SLAMF8) in TAMs and its impact on breast cancer cell proliferation.
Methods:
The SLAMF8 silencing in THP-1 cells was established by transfection with SLAMF8 shRNA lentiviral particles, and the THP-1 cells were induced to M0 macrophages or M2 macrophages. The M2 macrophage markers, CD11b+CD163, CD206, and IL-10, were measured by flow cytometry and Western blotting. The induced macrophages were cocultured with breast cancer cells (MCF-7 and MDA-MB-231) using a transwell insert. The viability and migration of cancer cells were measured using CCK-8 and transwell migration. The STAT6 and NF-κB pathways were measured using Western blotting. In vivo, mice were co-injected with breast cancer cells and the THP-1-derived macrophages to observe the tumor growth. The NF-κB pathway in tumor tissues was measured by immunohistochemistry and Western blotting.
Results:
The SLAMF8 silencing significantly downregulated the number of THP-1-derived M2 macrophages. The viability, migration, and the STAT6 and NF-κB pathways of breast cancer cells were significantly enhanced after co-culture with M2 macrophages compared to co-culture with M0 macrophages. However, the SLAMF8 silencing markedly suppressed the promoting effects of M2 macrophage co-culture on the above factors in cancer cells. In line with the in-vitro results, co-injection with M2 macrophages significantly promoted the tumor growth. Moreover, the SLAMF8 silencing in M2 macrophages downregulated the tumor growth compared with that of cancer cells co-injected with M2 macrophages without SLAMF8 silencing.
Conclusion:
This study showed that SLAMF8 silencing downregulated M2 macrophage polarization and weakened the promoting effects of M2 macrophages on breast cancer cells, suggesting a promising therapeutic strategy for breast cancer.
