fig1

Figure 1. Intercellular crosstalk between CAFs and ovarian cancer cells. Cancer cells, CAFs, and cisplatin can all contribute to the activation of normal fibroblasts. CAFs secrete factors and exosomes to alter key pathways involved in chemoresistance. Lastly, CAFs communicate through cell-cell contact, and certain subtypes such as myCAFs are known for their close proximity. CAFs: Cancer-associated fibroblasts; myCAFs: myofibroblastic cancer-associated fibroblasts; FAP: fibroblast activation protein α; α-SMA: α-smooth muscle actin; ECM-1: extracellular matrix protein-1; TGF-β: transforming growth factor-β; IFN1: interferon 1; IL-1β: interleukin-1β; STAT3: signal transducer and activator of transcription 3; PTEN: phosphatase and tensin homolog; SOCS6: suppressor of cytokine signaling; CDKN1A: cyclin-dependent kinase inhibitor 1A; Akt: protein kinase B.