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Fig. 3 | Journal of Biomedical Science

Fig. 3

From: A novel ligand-receptor relationship between families of ribonucleases and receptor tyrosine kinases

Fig. 3

A proposed model of the interplay between hRNase5/ANG and EGFR in modulating the pancreatic tumor microenvironment via an autocrine or paracrine pathway. Secretory hRNase5/ANG can originate from pancreatic tumor cells and bind to EGFR on the tumor cell surface in an autocrine manner. hRNase5/ANG can also be secreted from stroma matrix, including tumor-associated endothelial cells and tumor-associated fibroblasts, where it may bind to EGFR on the cell surface of endothelial cells and fibroblasts, respectively, and trigger EGFR signaling to form autocrine stimulation. In contrast, hRNase5/ANG derived from endothelial cells or fibroblasts may associate with cell surface EGFR of tumor cells, which may stimulate tumor-associated EGFR signaling in a paracrine manner. hRNase5/ANG secreted from tumor cells may interact with EGFR on endothelial cells or fibroblasts to play a role in angiogenesis or other processes. The scale of the diagram does not reflect the relative sizes of different molecules

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