scholarly journals Hepatocyte growth factor/c-metsignaling is required for stem-cell-mediated liver regeneration in mice

Hepatology ◽  
2012 ◽  
Vol 55 (4) ◽  
pp. 1215-1226 ◽  
Author(s):  
Tsuyoshi Ishikawa ◽  
Valentina M. Factor ◽  
Jens U. Marquardt ◽  
Chiara Raggi ◽  
Daekwan Seo ◽  
...  
Keyword(s):  
Stem Cell ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Liver Regeneration ◽  
Factor C ◽  
Hepatocyte Growth

scholarly journals Hepatocyte growth factor/c-met signaling pathway is required for efficient liver regeneration and repair

2004 ◽  
Vol 101 (13) ◽  
pp. 4477-4482 ◽  
Author(s):  
C.-G. Huh ◽  
V. M. Factor ◽  
A. Sanchez ◽  
K. Uchida ◽  
E. A. Conner ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Liver Regeneration ◽  
Signaling Pathway ◽  
Factor C ◽  
Hepatocyte Growth

scholarly journals HGF/c-Met Promote Renal Carcinoma Cancer Stem Cells Enrichment Through Upregulation of Cir-CCDC66

2020 ◽  
Vol 19 ◽  
pp. 153303381990111 ◽  
Author(s):  
Juhong Yang ◽  
Lei Yang ◽  
Shen Li ◽  
Ning Hu
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Growth Factor ◽  
Cancer Stem Cells ◽  
Cancer Stem Cell ◽  
Hepatocyte Growth Factor ◽  
Renal Carcinoma ◽  
Cell Enrichment ◽  
Factor C ◽  
Hepatocyte Growth

Increasing studies have suggested that circular RNAs play an important function in the process of numerous cancers. We aimed to investigate the possible role of cir-CCDC66 in renal carcinoma cancer. As cancer stem cells are responsible for the renal carcinoma cancer tumor growth and resistance to conventional therapy, we focus on the cir-CCDC66 influence on renal carcinoma cancer stem cells. In this study, we performed experiments in human renal tubular epithelial cell HK2 cells and several renal carcinoma cancer cancer cell lines. The results showed that cir-CCDC66 was upregulated not only in renal carcinoma cancer cancer cell lines but also in cancer stem cell spheres. What’s more, the results showed that cir-CCDC66 enhanced the cancer stem cell enrichment. Further mechanistic studies showed that hepatocyte growth factor/c-Met pathway was activated in cancer stem cell enrichment and responsible for the cir-CCDC66 upregulation. Inhibition of hepatocyte growth factor/c-Met could block cir-CCDC66-induced cancer stem cell enrichment. In conclusion, our research revealed a novel mechanism between hepatocyte growth factor/c-Met/cir-CCDC66 and cancer stem cell enrichment. We verified that cir-CCDC66 could be a promising biomarker and therapy target for renal carcinoma cancer treatment.

Abstract 1340: Disruption of a Hepatocyte Growth Factor/c-Met Receptor Autocrine Loop Severely Impairs the Potency of Pluripotent Adipose Stromal Cells

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Liying Cai ◽  
Brian H Johnstone ◽  
Zhong Liang ◽  
Dmitry Traktuev ◽  
Todd G Cook ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Rank Order ◽  
Residual Activity ◽  
Autocrine Loop ◽  
Major Mode ◽  
Factor C ◽  
Hepatocyte Growth

Background Paracrine stimulation of endogenous repair, rather than direct tissue regeneration, is increasingly accepted as a major mode of therapeutic stem and progenitor cell action; yet, this principle has not been fully established in vivo . Adipose-derived stem cells (ASCs) secrete many factors and promote reperfusion and tissue repair in ischemia models. RNA interference was used to silence the expression of the abundant protein, hepatocyte growth factor (HGF), to determine its contribution to ASC potency in vivo . Methods and Results Dual-cassette lentiviral vectors, expressing GFP and either a small hairpin RNA (shRNA) specific for HGF mRNA (shHGF) or a control sequence (shCtrl), were used to stably transduce ASCs (ASC-shHGF or ASC-shCtrl). ASC-shHGF secreted 5-fold less HGF, which resulted in a reduced ability of these cells to promote survival, proliferation and migration of mature and progenitor endothelial cells in vitro ( p <0.01). HGF knockdown also severely impaired the ability of ASCs to promote reperfusion in a mouse hindlimb ischemia model. Perfusion of the ischemic leg at 15 d in mice treated with ASC-Ctrl was 84±4%, compared to only 69±5% for ASC-shHGF ( p <0.05). Even so, ASC-shHGF retained residual activity as indicated by greater reperfusion ( p <0.05) than with saline treatment (58±6%). Capillary densities in ischemic tissues from each group followed a similar rank order (ASC-Ctrl>ASC-shHGF>saline) ( p <0.05 between each group). While there was no difference in total GFP + cells in ischemic limbs at 5 d after infusion, indicating similar homing potentials, 3-fold fewer ASC-shHGF were present in ischemic tissues at 15 d compared to ASC-shCtrl ( p <0.01). This was accompanied by an increase in TUNEL-positive ASC-shHGF cells (61 ± 0.1%) compared to ASC-Ctrl (41% ± 3.2%) in ischemic tissues at 5 d ( p <0.01); suggesting that attenuated potency of ASC-shHGF was related to reduced survival in ischemic tissues. Conclusions These results indicate that secretion of HGF is critically important for ASC potency. In addition to promoting endogenous repair, the data suggest that an important effect of HGF is autocrine promotion of ASC survival in ischemic tissue. Enhanced donor cell survival is an important goal for increasing the efficacy of cell therapy.

Hepatocyte Growth Factor Stimulates Liver Regeneration and Elevates Blood Protein Level in Normal and Partially Hepatectomized Rats

1995 ◽  
Vol 117 (5) ◽  
pp. 1105-1112 ◽  
Author(s):  
Takehisa Ishii ◽  
Maki Sato ◽  
Keiko Sudo ◽  
Masayuki Suzuki ◽  
Hiroshi Nakai ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Liver Regeneration ◽  
Protein Level ◽  
Blood Protein ◽  
Hepatocyte Growth
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