scholarly journals Lipopolysaccharide inhibition of glucose production through the Toll-like receptor-4, myeloid differentiation factor 88, and nuclear factor κb pathway

Hepatology ◽  
2009 ◽  
Vol 50 (2) ◽  
pp. 592-600 ◽  
Author(s):  
Carl F. Raetzsch ◽  
Natasha L. Brooks ◽  
J. McKee Alderman ◽  
Kelli S. Moore ◽  
Peter A. Hosick ◽  
...  
Keyword(s):  
Glucose Production ◽  
Nuclear Factor Κb ◽  
Myeloid Differentiation ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Differentiation Factor ◽  
Myeloid Differentiation Factor 88 ◽  
Myeloid Differentiation Factor

scholarly journals High mobility group box 1/toll-like receptor 4/myeloid differentiation factor 88 signaling promotes progression of gastric cancer

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769431 ◽  
Author(s):  
Yanqiu Yue ◽  
Tao Zhou ◽  
Yanjing Gao ◽  
Zongli Zhang ◽  
Li Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Nuclear Factor Kappa B ◽  
High Mobility ◽  
High Mobility Group ◽  
Myeloid Differentiation ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Differentiation Factor ◽  
Myeloid Differentiation Factor 88 ◽  
Myeloid Differentiation Factor

High mobility group box 1 and toll-like receptor 4/myeloid differentiation factor 88 signaling pathway have been indicated to have oncogenic effects in many cancers. However, the role of high mobility group box 1/toll-like receptor 4/myeloid differentiation factor 88 signaling pathway in the development of gastric cancer remains unclear. In this study, we demonstrated that high mobility group box 1, toll-like receptor 4, and myeloid differentiation factor 88 were overexpressed in gastric cancer tumors compared with the adjacent non-tumor tissues. The overexpression of high mobility group box 1, toll-like receptor 4, and myeloid differentiation factor 88 were correlated with tumor-node-metastasis stage (p = 0.0068, p = 0.0063, p = 0.0173) and lymph node metastasis (p = 0.0272, p = 0.0382, and p = 0.0495). Furthermore, we observed that knockdown of high mobility group box 1 by high mobility group box 1-small interfering RNA suppressed the expression of toll-like receptor 4 and myeloid differentiation factor 88. Blockage of high mobility group box 1/toll-like receptor 4/myeloid differentiation factor 88 signaling by high mobility group box 1-small interfering RNA resulted in elevation of apoptotic ratio and inhibition of cell growth, migration, and invasion by upregulating Bax expression and downregulating Bcl-2, matrix metalloproteinase-2, nuclear factor kappa B/p65 expression, and the nuclear translocation of nuclear factor kappa B/p65 in gastric cancer cells. Our findings suggest that high mobility group box 1/toll-like receptor 4/myeloid differentiation factor 88 signaling pathway may contribute to the development and progression of gastric cancer via the nuclear factor kappa B pathway and it also represents a novel potential therapeutic target for gastric cancer.

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