scholarly journals Regulation of MET receptor tyrosine kinase signaling by suppressor of cytokine signaling 1 in hepatocellular carcinoma

Oncogene ◽  
2015 ◽  
Vol 34 (46) ◽  
pp. 5718-5728 ◽  
Author(s):  
Y Gui ◽  
M Yeganeh ◽  
Y-C Donates ◽  
W-S Tobelaim ◽  
W Chababi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Cytokine Signaling ◽  
Kinase Signaling ◽  
Met Receptor ◽  
Suppressor Of Cytokine Signaling ◽  
Tyrosine Kinase Signaling ◽  
Met Receptor Tyrosine Kinase

scholarly journals Met Receptor Tyrosine Kinase Signaling Induces Secretion of the Angiogenic Chemokine Interleukin-8/CXCL8 in Pancreatic Cancer

PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e40420 ◽  
Author(s):  
Kristen S. Hill ◽  
Ivana Gaziova ◽  
Lindsay Harrigal ◽  
Yvette A. Guerra ◽  
Suimin Qiu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Interleukin 8 ◽  
Kinase Signaling ◽  
Met Receptor ◽  
Tyrosine Kinase Signaling ◽  
Met Receptor Tyrosine Kinase

scholarly journals Dorsal Ruffle Microdomains Potentiate Met Receptor Tyrosine Kinase Signaling and Down-regulation

2010 ◽  
Vol 285 (32) ◽  
pp. 24956-24967 ◽  
Author(s):  
Jasmine V. Abella ◽  
Christine A. Parachoniak ◽  
Veena Sangwan ◽  
Morag Park
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Kinase Signaling ◽  
Met Receptor ◽  
Down Regulation ◽  
Tyrosine Kinase Signaling ◽  
Met Receptor Tyrosine Kinase

scholarly journals lncRNA HOTAIR overexpression promotes hybrid epithelial/mesenchymal phenotype through suppression of c-Met Receptor Tyrosine Kinase Signaling in Hepatocellular Carcinoma Cells

2020 ◽  
Author(s):  
Hande Topel ◽  
Ezgi Bagirsakci ◽  
Dehan Comez ◽  
Gulsun Bagci ◽  
Gulcin Cakan-Akdogan ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tyrosine Kinase ◽  
Cell Fate ◽  
Receptor Tyrosine Kinase ◽  
Biological Significance ◽  
Met Receptor ◽  
Mesenchymal Transition ◽  
Met Receptor Tyrosine Kinase ◽  
Lncrna Hotair

Abstract Background: Epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET) are both reversible processes, and regulation of phenotypical transition is very important for progression of several cancers including hepatocellular carcinoma (HCC). Recently, it is defined that cancer cells can attain a hybrid epithelial/mesenchymal (hybrid E/M) phenotype. Cells with hybrid E/M phenotype comprise mixed epithelial and mesenchymal properties, they can be more resistant to therapeutics and also more capable of initiating metastatic lesions. However, the mechanisms regulating hybrid E/M in HCC are not well described yet. In this study, we investigated the role of the potential crosstalk between lncRNA HOTAIR and c-Met receptor tyrosine kinase, which are two essential regulators of EMT and MET, in acquiring of hybrid E/M phenotype in HCC.Methods: Expression of c-Met and HOTAIR were defined in HCC cell lines and patient tissues through HCC progression. lncRNA HOTAIR was overexpressed in SNU-449 cells and its effects on c-Met signaling were analyzed. c-Met was overexpressed in SNU-398 cells and its effect on HOTAIR expression was analyzed. Biological significance of HOTAIR/c-Met interplay was defined in means of adhesion, proliferation, motility behavior, invasion, spheroid formation and metastatic ability. Effect of ectopic HOTAIR expression on phenotype was defined with investigation of molecular epithelial and mesenchymal traits.Results: In vitro and in vivo experiments verified the pivotal role of lncRNA HOTAIR in acquisition of hybrid E/M phenotype through modulating c-Met and its membrane co-localizing partner Caveolin-1 expression, activation and membrane organization to cope with the rate limiting steps of metastasis such as survival in adhesion independent microenvironment, escaping from anoikis and resisting to fluidic shear stress (FSS) in HCC.Conclusions: Our work provides the first evidence suggesting a role for lncRNA HOTAIR in the modulation of c-Met to promote hybrid E/M phenotype. The balance between lncRNA HOTAIR and c-Met might be critical for cell fate decision and metastatic potential of HCC cells.

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