Abstract
Recent insights into the molecular and cellular mechanisms underlying cancer development have revealed the tumor microenvironment (TME) immune cells to functionally affect the development and progression of breast cancer. However, insufficient evidence of TME immune modulators limit the clinical application of immunotherapy for advanced and metastatic breast cancers. Intercellular STAT3 activation of immune cells plays a central role in breast cancer TME immunosuppression and distant metastasis. Accumulating evidence suggests that targeting STAT3 and/or in combination with radiotherapy may enhance anti-cancer immune responses and rescue the systemic immunologic microenvironment in breast cancer. Indeed, apart from its oncogenic role in tumor cells, the functions of STAT3 in TME of breast cancer involve multiple types of immunosuppression and is associated with tumor cell metastasis. In this review, we summarize the available information on the functions of STAT3-related immune cells in TME of breast cancer, as well as the specific upstream and downstream targets. Additionally, we provide insights about the potential immunosuppression mechanisms of each type of evaluated immune cells.5xNT5_6Jt5-SmMPvLS1tBCVideo abstract
Highlights
Breast cancer is one of the most prevalent type of gynecological cancer across the globe
Previous studies demonstrate that Signal transducer and activator of transcription 3 (STAT3) activation not merely act as a predictive biomarker for downregulated immune cells response, and the type of immunomodulator that is strongly associated with programmed death ligand 1 (PD-L1) expression in the tumor microenvironment (TME) of breast cancer [15, 29, 200]
Conclusions and future perspectives Numerous studies support the role of STAT3 in immune cells and dictates the immunomodulatory effects to the TME of breast cancer
Summary
Breast cancer is one of the most prevalent type of gynecological cancer across the globe. The S100A8/A9-mediated ROS suppression was reported to improve the CD4+ T cell accumulation in TME of breast cancer, which has been known to be regulated in STAT3-dependent mechanism in MDSCs [54, 58, 59, 61].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
