fig2

Figure 2. CAFs create a biomechanical niche for CSCs, mediating resistance. Integrins interact with collagen produced by CAFs and activate FAK-Src signaling or initiate cytoskeletal deformation and subsequent AIRE-mediated transcription of stemness factors, enhancing the stemness of CSCs. When the ECM becomes stiffer and exerts excessive stress on CSCs, DDR2 on CSCs receives the biomechanical signal and causes cell cycle arrest via the STAT1/P27 axis, facilitating CSCs into a dormant status. CAFs: Cancer-associated fibroblasts; CSCs: cancer stem cells; FAK: focal adhesion kinase; AIRE: autoimmune regulator gene; ECM: extracellular matrix; DDR2: discoidin domain receptor 2; STAT1: signal transducer and activator of transcription 1; YAP1: Yes1-associated transcriptional regulator 1; WNT: Wnt family member; NOTCH: neurogenic locus notch homolog protein.