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Tytuł pozycji:

Proline-Rich Tyrosine Kinase 2 (Pyk2) Promotes Cell Motility of Hepatocellular Carcinoma through Induction of Epithelial to Mesenchymal Transition

Tytuł :
Proline-Rich Tyrosine Kinase 2 (Pyk2) Promotes Cell Motility of Hepatocellular Carcinoma through Induction of Epithelial to Mesenchymal Transition
Autorzy :
Chris K Sun
Kevin T Ng
Zophia X Lim
Qiao Cheng
Chung Mau Lo
Ronnie T Poon
Kwan Man
Nathalie Wong
Sheung Tat Fan
Pokaż więcej
Temat :
Epithelial-Mesenchymal Transition - physiology
Research Article
Biology
Focal Adhesion Kinase 2 - metabolism - physiology
Medicine
Basic Cancer Research
digestive system diseases
Oncology
Cell Motility
Liver Neoplasms - enzymology - pathology - ultrastructure
Cell Movement - physiology
Gastrointestinal Tumors
Science
Carcinoma, Hepatocellular - enzymology - pathology - ultrastructure
Cancers and Neoplasms
Biophysics
Hepatocellular Carcinoma
Źródło :
PLoS ONE, Vol 6, Iss 4, p e18878 (2011)
Wydawca :
Public Library of Science, 2011.
Rok publikacji :
2011
Oryginalny identyfikator :
pmc: PMC3080371
pmid: 21533080
Język :
English
ISSN :
1932-6203
DOI :
10.1371/journal.pone.0018878
Aims: Proline-rich tyrosine kinase 2 (Pyk2), a non-receptor tyrosine kinase of the focal adhesion kinase (FAK) family, is up-regulated in more than 60% of the tumors of hepatocellular carcinoma (HCC) patients. Forced overexpression of Pyk2 can promote the proliferation and invasion of HCC cells. In this study, we aimed to explore the underlying molecular mechanism of Pyk2-mediated cell migration of HCC cells. Methodology/Principal Findings: We demonstrated that Pyk2 transformed the epithelial HCC cell line Hep3B into a mesenchymal phenotype via the induction of epithelial to mesenchymal transition (EMT), signified by the up-regulation of membrane ruffle formation, activation of Rac/Rho GTPases, down-regulation of epithelial genes E-cadherin and cytokeratin as well as promotion of cell motility in presence of lysophosphatidic acid (LPA). Suppression of Pyk2 by overexpression of dominant negative PRNK domain in the metastatic HCC cell line MHCC97L transformed its fibroblastoid phenotype to an epithelial phenotype with up-regulation of epithelial genes, down-regulation of mesenchymal genes N-cadherin and STAT5b, and reduction of LPA-induced membrane ruffle formation and cell motility. Moreover, overexpression of Pyk2 in Hep3B cells promoted the phosphorylation and localization of mesenchymal gene Hic-5 onto cell membrane while suppression of Pyk2 in MHCC97L cells attenuated its phosphorylation and localization. Conclusion: These data provided new evidence of the underlying mechanism of Pyk2 in controlling cell motility of HCC cells through regulation of genes associated with EMT. © 2011 Sun et al.

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