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Xian-Feng Wang

Researcher at Sun Yat-sen University

Publications -  9
Citations -  930

Xian-Feng Wang is an academic researcher from Sun Yat-sen University. The author has contributed to research in topics: Macrophage polarization & Snail. The author has an hindex of 8, co-authored 9 publications receiving 706 citations. Previous affiliations of Xian-Feng Wang include Centers for Disease Control and Prevention.

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TGF-β induces M2-like macrophage polarization via SNAIL-mediated suppression of a pro-inflammatory phenotype

TL;DR: It is found that TGF-β induces a M2-like phenotype characterized by up-regulation of the anti-inflammatory cytokine IL-10, and down- regulation of the pro- inflammatory cytokines TNF-α and IL-12, which suggests a potential therapeutic target for antitumor immunity.
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Epithelial-mesenchymal transition (EMT) induced by TNF-α requires AKT/GSK-3β-mediated stabilization of snail in colorectal cancer.

TL;DR: It is revealed that AKT/GSK-3β-mediated stabilization of Snail is required for TNFα-induced EMT in CRC cells, and this study provides a better understanding of inflammation-induced CRC metastasis.
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The role of indoleamine 2,3-dioxygenase (IDO) in immune tolerance: focus on macrophage polarization of THP-1 cells.

TL;DR: The results suggested that the expression intensity of IDO modulates macrophage differentiation, which support the counter-regulatory role for IDO with regarding to the polarization of macrophages to restrain excessive or inappropriate immune activation in inflammatory or tumor microenvironment.
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Stabilization of Snail through AKT/GSK-3β signaling pathway is required for TNF-α-induced epithelial-mesenchymal transition in prostate cancer PC3 cells.

TL;DR: It is shown that stabilization of Snail via AKT/GSK-3β signaling pathway is required for TNFα-induced EMT in prostate cancer cells, and this study offers a better understanding of TNF α-induced metastasis and provides an effective therapeutic strategy for prostate cancer treatment.
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Deubiquitinase Inhibition of 19S Regulatory Particles by 4-Arylidene Curcumin Analog AC17 Causes NF-κB Inhibition and p53 Reactivation in Human Lung Cancer Cells

TL;DR: Treatment with AC17 suppresses tumor growth in a manner associated with proteasome inhibition, NF-κB blockage, and p53 reactivation in a murine xenograft model of human lung cancer A549, suggesting that 4-arylidene curcumin analogs are novel 19S deubiquitinase inhibitors with great potential for anticancer drug development.