Tumor necrosis factor-α modulates epithelial mesenchymal transition mediators ZEB2 and S100A4 to promote cholangiocarcinoma progression

2014 ◽  
Vol 21 (9) ◽  
pp. 703-711 ◽  
Author(s):  
Anchalee Techasen ◽  
Nisana Namwat ◽  
Watcharin Loilome ◽  
Kassaporn Duangkumpha ◽  
Anucha Puapairoj ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Factor Α ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α) stimulates the epithelial–mesenchymal transition regulator Snail in cholangiocarcinoma

2012 ◽  
Vol 29 (5) ◽  
pp. 3083-3091 ◽  
Author(s):  
Anchalee Techasen ◽  
Nisana Namwat ◽  
Watcharin Loilome ◽  
Pornpan Bungkanjana ◽  
Narong Khuntikeo ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Tumor Necrosis Factor-α Stimulates the Epithelial-to-Mesenchymal Transition of Human Colonic Organoids

2003 ◽  
Vol 14 (5) ◽  
pp. 1790-1800 ◽  
Author(s):  
Richard C. Bates ◽  
Arthur M. Mercurio
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Progression ◽  
Colon Carcinoma ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Transforming Growth Factor ◽  
Mesenchymal Transition ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

An epithelial-mesenchymal transition (EMT) characterizes the progression of many carcinomas and it is linked to the acquisition of an invasive phenotype. Given that the tumor microenvironment is an active participant in tumor progression, an important issue is whether a reactive stroma can modulate this process. Using a novel EMT model of colon carcinoma spheroids, we demonstrate that their transforming-growth factor-β1 (TGF-β)-induced EMT is accelerated dramatically by the presence of activated macrophages, and we identify tumor necrosis factor-α (TNF-α) as the critical factor produced by macrophages that accelerates the EMT. A synergy of TNF-α and TGF-β signaling promotes a rapid morphological conversion of the highly organized colonic epithelium to dispersed cells with a mesenchymal phenotype, and this process is dependent on enhanced p38 MAPK activity. Moreover, exposure to TNF-α stimulates a rapid burst of ERK activation that results in the autocrine production of this cytokine by the tumor cells themselves. These results establish a novel role for the stroma in influencing EMT in colon carcinoma, and they identify a selective advantage to the stromal presence of infiltrating leukocytes in regulating malignant tumor progression.

scholarly journals MicroRNA signature of inflamed lymphatic endothelium and role of miR-9 in lymphangiogenesis and inflammation

2015 ◽  
Vol 309 (10) ◽  
pp. C680-C692 ◽  
Author(s):  
Sanjukta Chakraborty ◽  
David C. Zawieja ◽  
Michael J. Davis ◽  
Mariappan Muthuchamy
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Fine Tuning ◽  
Vegf Receptor ◽  
Mesenchymal Transition ◽  
Factor Α ◽  
Endothelial Mesenchymal Transition ◽  
Necrosis Factor

The lymphatics have emerged as critical players in the progression and resolution of inflammation. The goal of this study was to identify specific microRNAs (miRNAs) that regulate lymphatic inflammatory processes. Rat mesenteric lymphatic endothelial cells (LECs) were exposed to the proinflammatory cytokine tumor necrosis factor-α for 2, 24, and 96 h, and miRNA profiling was carried out by real-time PCR arrays. Our data demonstrate a specific set of miRNAs that are differentially expressed (>1.8-fold and/or P < 0.05) in LECs in response to tumor necrosis factor-α and are involved in inflammation, angiogenesis, endothelial-mesenchymal transition, and cell proliferation and senescence. We further characterized the expression of miRNA 9 (miR-9) that was induced in LECs and in inflamed rat mesenteric lymphatics. Our results showed that miR-9 overexpression significantly repressed NF-κB expression and, thereby, suppressed inflammation but promoted LEC tube formation, as well as expression of the prolymphangiogenic molecules endothelial nitric oxide synthase and VEGF receptor type 3. LEC viability and proliferation and endothelial-mesenchymal transition were also significantly induced by miR-9. This study provides the first evidence of a distinct profile of miRNAs associated with LECs during inflammation. It also identifies the critical dual role of miR-9 in fine-tuning the balance between lymphatic inflammatory and lymphangiogenic pathways.

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