SLAMF1 expression in breast cancer cells delays tumor growth in vivo.

Signaling lymphocytic activation molecule (SLAM) family receptors are widely expressed on immune cells, often acting as self-ligands and playing crucial roles in cellular communication and adhesion, thereby modulating immune responses. Several studies have demonstrated that SLAM family receptors are associated with potential immune checkpoints on T cells and play a role in tumor immunity in various cancers. However, the effect of SLAMF1 expression in tumors has been rarely investigated. Here, we confirmed SLAMF1 expression using tissue microarray analysis in breast cancer tissues with diverse pathological characteristics and subtypes. Additionally, SLAMF1 expression in triple-negative breast cancer (TNBC) cells was analyzed using flow cytometry and real-time PCR. Public clinical data analysis suggests that a positive correlation exists between SLAMF1 expression and overall survival and that SLAMF1 levels are slightly increased in patients with breast cancer who received radiation therapy. Similarly, when TNBC cells were irradiated, SLAMF1 expression specifically increased compared to that in non-irradiated cells. To study the biological function of SLAMF1 in mice, we established 4T1-SLAMF1 overexpressing a stable cell line. In the 4T1 syngenetic tumor model, SLAMF1 overexpression triggered strong infiltrating-CD8+ T cell responses and significantly reduced the tumor growth. Our results provide clear evidence for SLAMF1 expression in breast cancer and provide insights into the recent advances in SLAM-based targeted immunotherapies.