FAP Promotes Immunosuppression by Cancer-Associated Fibroblasts in the Tumor Microenvironment via STAT3–CCL2 Signaling

• Published in: Cancer research (Chicago, Ill.) Vol. 76; no. 14; pp. 4124 - 4135
• Main Authors: Yang, Xuguang, Lin, Yuli, Shi, Yinghong, Li, Bingji, Liu, Weiren, Yin, Wei, Dang, Yongjun, Chu, Yiwei, Fan, Jia, He, Rui
• Format: Journal Article
• Language: English
• Published: United States 15.07.2016
• Subjects: Animals; Cancer-Associated Fibroblasts - physiology; Cell Movement; Chemokine CCL2 - physiology; Female; Focal Adhesion Protein-Tyrosine Kinases - physiology; Gelatinases - physiology; Immune Tolerance; Janus Kinase 2 - physiology; Membrane Proteins - physiology; Mice; Mice, Inbred C57BL; Receptors, Urokinase Plasminogen Activator - physiology; Serine Endopeptidases - physiology; Signal Transduction - physiology; STAT3 Transcription Factor - physiology; Tumor Microenvironment

Cancer-associated fibroblasts (CAF) are components of the tumor microenvironment whose contributions to malignant progression are not fully understood. Here, we show that the fibroblast activation protein (FAP) triggers induction of a CAF subset with an inflammatory phenotype directed by STAT3 activ...