scholarly journals Importance of osteoprotegrin and receptor activator of nuclear factor κB in breast cancer response to hepatocyte growth factor and the bone microenvironment in vitro

2016 ◽  
Vol 48 (3) ◽  
pp. 919-928 ◽  
Author(s):  
SIONED OWEN ◽  
ANDREW J. SANDERS ◽  
MALCOLM D. MASON ◽  
WEN G. JIANG
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Bone Microenvironment ◽  
Receptor Activator ◽  
Hepatocyte Growth

scholarly journals Hepatocyte Growth Factor Exerts Its Anti-Inflammatory Action by Disrupting Nuclear Factor-κB Signaling

2008 ◽  
Vol 173 (1) ◽  
pp. 30-41 ◽  
Author(s):  
Myrto Giannopoulou ◽  
Chunsun Dai ◽  
Xiaoyue Tan ◽  
Xiaoyan Wen ◽  
George K. Michalopoulos ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Anti Inflammatory ◽  
Hepatocyte Growth ◽  
Inflammatory Action

scholarly journals In VitroandIn VivoEffects of Suppressor of Cytokine Signalling 7 Knockdown in Breast Cancer: The Influence on Cellular Response to Hepatocyte Growth Factor

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Walid Sasi ◽  
Lin Ye ◽  
Wen G. Jiang ◽  
Anup K. Sharma ◽  
Kefah Mokbel
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Xenograft Growth ◽  
And Migration ◽  
Hepatocyte Growth

Purpose. Suppressor of cytokine signaling 7 (SOCS7) is a member of the SOCS family and is known to interact with phospholipase Cγ-1 (PLCγ-1), a key downstream mediator of the hepatocyte growth factor (HGF)/C-MET axis. Here, we report our observations of the effect of knocking down SOCS7 gene on the behaviour of breast cancer cells bothin vitroandin vivoand to elucidate whether this involves HGF/C-MET pathway using the PLCγ-1 blocker U73122.Methods. MCF7 and MDA-MB-231 breast cancer cells were transfected with anti-SOCS7 ribozymal transgene, to create sublines with SOCS7 knockdown. Thein vitrogrowth and migration of the cells were evaluated in basic conditions and with HGF and U73122 treatment using growth assays, scratch-wound, and electrical cell impedance sensing (ECIS) migration assays. MCF7 and MDA-MB-231in vivotumour xenograft growth were also studied.Results. Basalin vitrogrowth and migration of both cellular lines and thein vivoMCF7 xenograft growth were significantly enhanced with SOCS7 knockdown.In vitroHGF treatment has further influenced the growth and migration when SOCS7 gene was knocked-down in both cellular lines(P<0.05). PLCγ-1 pharmacological inhibition of the HGF/C-MET cascade during theirin vitrogrowth and migration seemed to only occur when SOCS7 gene was knocked down.Conclusions. We report a unique regulatory role for SOCS7 in controlling the malignant behaviour of breast cancer lines MCF7 and MDA-MB-231in vitroand the MCF7 tumour xenograftsin vivo. We also report a regulatory role for SOCS7 during thein vitroHGF-induced growth and migration in these cells as HGF treatment and SOCS7 loss have synergistically enhanced these functions. This SOCS7 knockdown-attributed effect could be due to a precise anti-PLCγ-1 role.

scholarly journals Targeting hepatocyte growth factor in epithelial–stromal interactions in an in vitro experimental model of human periodontitis

Odontology ◽  
2021 ◽  
Author(s):  
Yoko Yamaguchi ◽  
Akira Saito ◽  
Masafumi Horie ◽  
Akira Aoki ◽  
Patrick Micke ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Experimental Studies ◽  
Three Dimensional ◽  
Collagen Gel ◽  
Neutralizing Antibody ◽  
Chronic Inflammatory Disease ◽  
Collagen Degradation ◽  
Hepatocyte Growth

AbstractPeriodontitis is a chronic inflammatory disease leading to progressive connective tissue degradation and loss of the tooth-supporting bone. Clinical and experimental studies suggest that hepatocyte growth factor (HGF) is involved in the dysregulated fibroblast–epithelial cell interactions in periodontitis. The aim of this study was to explore effects of HGF to impact fibroblast-induced collagen degradation. A patient-derived experimental cell culture model of periodontitis was applied. Primary human epithelial cells and fibroblasts isolated from periodontitis-affected gingiva were co-cultured in a three-dimensional collagen gel. The effects of HGF neutralizing antibody on collagen gel degradation were tested and transcriptome analyses were performed. HGF neutralizing antibody attenuated collagen degradation and elicited expression changes of genes related to extracellular matrix (ECM) and cell adhesion, indicating that HGF signaling inhibition leads to extensive impact on cell–cell and cell–ECM interactions. Our study highlights a potential role of HGF in periodontitis. Antagonizing HGF signaling by a neutralizing antibody may represent a novel approach for periodontitis treatment.

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