Autophagy in host stromal fibroblasts supports tumor desmoplasia

Figures & data

Figure 1. Autophagy in stromal fibroblasts supports desmoplasia and tumor growth in trans. Enhanced COL1A deposition and inflammatory cell recruitment are hallmarks of tumor desmoplasia. Autophagy in stromal fibroblasts promotes the degradation of misfolded type 1 pro-collagen (PC1), which maintains cellular proteostasis and enables the efficient secretion of COL1A necessary for creating the stiff fibrotic matrix found in desmoplastic stroma. At the same time, stromal fibroblast autophagy facilitates the secretion of IL6 and other pro-angiogenic and immune-modulatory cytokines. This enables the recruitment of both innate and adaptive immune cells to the tumor microenvironment (TME). Collectively, these pathways create a hospitable TME for tumor cell proliferation and survival. As a result, stromal fibroblast autophagy promotes tumor growth