39 research outputs found

    Radio Astronomy

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    Contains reports on one research project.National Aeronautics and Space Administration (Contract NAS5-21980

    Radio Astronomy

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    Contains reports on two research projecst.California Institute of Technology Contract 952568Sloan Fund for Basic Research (M.I. T. Grant 241

    Radio Astronomy

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    Contains reports on two research projects.California Institute of Technology (Contract 952568)U. S. Air Force Air Force Systems Command (Contract F33615-72-C-2129

    Radio Astronomy

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    Contains reports on three research projects.National Aeronautics and Space Administration (Grant NGL 22-009-016)National Aeronautics and Space Administration (Grant NGL 22-009-421)National Science Foundation (Grant GP-20769)California Institute of Technology Contract 952568Sloan Fund for Basic Research (M. I. T. Grant 241

    Radio Astronomy

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    Contains reports on four research projects.National Aeronautics and Space Administration (Grant NGL 22-009-016)National Aeronautics and Space Administration (Grant NGR 22-009-421)National Science Foundation (Grant GP-20769)National Science Foundation (Grant GP-21348)California Institute of Technology Contract 952568Sloan Fund for Basic Research (M. I. T. Grant 241

    Radio Astronomy

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    Contains reports on three research project.National Science Foundation (Grant GP-21348A#2)California Institute of Technology (Contract 952568)National Aeronautics and Space Administration (Grant NGR 22-009-421)U. S. Air Force - Electronic Systems Division (Contract F19628-73-C-0196

    Radio Astronomy

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    Contains reports on eight research projects.National Aeronautics and Space Administration, Langley Research Center (Contract NAS1-10693)California Institute of Technology Contract 952568Joint Services Electronics Programs (U. S. Army, U.S. Navy, and U. S. Air Force) under Contract DAAB07-71-C-0300National Science Foundation (Grant GP-20769A#1)National Science Foundation (Grant GP-21348A#1

    Radio Astronomy

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    Contains reports on four research projects.Joint Services Electronics Program (Contract DAAB07-71-C-0300)California Institute of Technology (Contract 952568)National Aeronautics and Space Administration (Contract NAS1-10693)National Science Foundation (Grant GP-21348A#2

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

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    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.published_or_final_versio
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