FIGURE

Fig. 7

ID

ZDB-FIG-240115-7

Publication

Li et al., 2024 - ANGPTL4 accelerates ovarian serous cystadenocarcinoma carcinogenesis and angiogenesis in the tumor microenvironment by activating the JAK2/STAT3 pathway and interacting with ESM1

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Fig. 7

A model of the molecular mechanism by which ANGPTL4 promotes OC development and progression. A OC is a type of tumor with a rich blood supply. B There are many angiogenic factors in the tumor microenvironment of OC. C A variety of cells in the tumor microenvironment can take up these angiogenesis factors in a variety of ways to produce different pathophysiological effects. D ANGPTL4 can promote the proliferation and migration of OC cells by activating the JAK-STAT3 pathway, and ESM1 can bind ANGPTL4 and stabilize the binding of ANGPTL4 to LPL, thus promoting lipid accumulation and accelerating the proliferation and migration of OC cells. ANGPTL4 can also promote endothelial cell proliferation and migration through the JAK-STAT3 signaling pathway. ESM1 can inhibit the binding of ANGPTL4 to integrin α5β1 to increase vascular stability. Moreover, ESM1 promotes angiogenesis in the ovarian cancer microenvironment by binding to ANGPTL4 to inhibit its destruction of VE-cadherin-mediated tight junctions. E The molecular mechanism might be attributed to the interaction of ESM1 and ANGPTL4.

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Acknowledgments

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