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How does hepatoma-derived growth factor (HDGF) regulate EMT? 


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Hepatoma-derived growth factor (HDGF) plays a significant role in regulating EMT through various mechanisms. In prostate cancer, HDGF knockdown inhibits EMT by upregulating E-cadherin and downregulating N-cadherin, Vimentin, Snail, and Slug proteins . Additionally, HDGF promotes EMT in hepatocellular carcinoma by upregulating HGF and c-Met expression, leading to increased migration of tumor cells . Furthermore, in gastric cancer, HDGF enhances tumor cell survival and invasive motility by recruiting mesenchymal stem cells and promoting their differentiation into myofibroblast-like cells . These findings collectively demonstrate that HDGF influences EMT by modulating key proteins and pathways involved in cellular migration, invasion, and metastasis in various types of cancer.

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Hepatoma-derived growth factor (HDGF) promotes differentiation of human mesenchymal stem cells to myofibroblast-like cells, contributing to EMT in gastric cancer progression.
Activated monocyte-derived TNF-α upregulates HGF/c-Met, triggering EMT in hepatoma cells by increasing HGF and c-Met expression, promoting EMT markers, and enhancing cell migration via HGF-c-Met signaling.
Not addressed in the paper.
HDGF regulates EMT by downregulating mesenchymal markers (N-cadherin, Vimentin, Snail, Slug) and upregulating the epithelial marker E-cadherin, inhibiting migration and invasion in prostate cancer cells.

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