Research Progress of Oncostatin M in Microenvironment Regulation and Metastasis of Breast Cancer

Oncostatin M (OSM), a cytokine belonging to the interleukin-6 family, plays a crucial role in modulating the breast cancer microenvironment and facilitating metastasis. It influences tumor cells directly, as well as immune cells, stromal cells, and vascular endothelial cells indirectly, thereby creating a complex interactive network that enhances tumor invasion and spread. The high expression of OSM in breast cancer is positively correlated with tumor grade, stage and metastasis, and enhances the invasion ability and chemotherapy resistance of tumor cells by activating JAK/STAT3 and PI3K/AKT signal pathways. In addition, OSM induced tumor-associated macrophages (TAMs) to polarize to M2 type, weakened the function of CD8^+T cells, promoted the proliferation of myeloid-derived suppressor cells (MDSCs), and inhibited the anti-tumor immune response. At the same time, it activates cancer-associated fibroblasts (CAFs) and promotes angiogenesis, supporting the formation of tumor matrix and metastasis niches. OSM signals are cross-regulated with multiple channels, forming a transfer-promoting loop. Clinical studies have shown that the high expression of OSM is related to the shortened survival period of patients, and intervention studies have verified its function of promoting metastasis. Nevertheless, the exact mechanism of OSM in breast cancer needs to be further explored, especially its potential as a therapeutic target and its application prospect as an inhibitor or antagonist, which provides a direction for future research.