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Deficiency in VHR/DUSP3, a suppressor of focal adhesion kinase, reveals its role in regulating cell adhesion and migration.
Chen, Y-R; Chou, H-C; Yang, C-H; Chen, H-Y; Liu, Y-W; Lin, T-Y; Yeh, C-L; Chao, W-T; Tsou, H-H; Chuang, H-C; Tan, T-H.
Affiliation
  • Chen YR; Institute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
  • Chou HC; Institute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
  • Yang CH; Institute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
  • Chen HY; Institute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
  • Liu YW; Department of Life Science, Tunghai University, Taichung, Taiwan.
  • Lin TY; Institute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
  • Yeh CL; Institute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
  • Chao WT; Institute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
  • Tsou HH; Department of Life Science, Tunghai University, Taichung, Taiwan.
  • Chuang HC; Division of Biostatistics and Bioinformatics, Institute of Population Health Sciences, National Health Research Institutes, Zhunan, Taiwan.
  • Tan TH; Graduate Institute of Biostatistics, College of Public Health, China Medical University, Taichung, Taiwan.
Oncogene ; 36(47): 6509-6517, 2017 11 23.
Article in En | MEDLINE | ID: mdl-28759036
ABSTRACT
Vaccinia H1-related phosphatase (VHR/DUSP3) is a member of the dual-specificity phosphatase family. Deregulation of VHR is observed in various malignant diseases. We identified focal adhesion kinase (FAK) as a VHR-interacting molecule. Over-expression of VHR decreased tyrosine phosphorylation of FAK and decreasing VHR promoted FAK tyrosine phosphorylation. In vitro assays proved that recombinant VHR directly dephosphorylated FAK and paxillin. VHR-knockout mice did not have obvious abnormality; however, VHR-knockout cells showed decreased expression of integrins and FAK but stronger FAK and paxillin phosphorylation upon attachment to fibronectin. Additionally, VHR-knockout fibroblast and lung epithelial cells had elevated ligand-induced epidermal growth factor receptor (EGFR) phosphorylation. Inducible expression of VHR suppressed directional cell migration, and VHR deficiency resulted in a higher cell migratory ability. VHR-knockout cells have stronger FAK phosphorylation in cell adhesions, long-lasting trailing ends and slower turnover of focal adhesions. These collective data indicate that VHR is a FAK phosphatase and participates in regulating the formation and disassembly of focal adhesions.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Cell Adhesion / Cell Movement / Focal Adhesion Kinase 1 / Dual Specificity Phosphatase 3 Type of study: Prognostic_studies Limits: Animals / Humans Language: En Journal: Oncogene Journal subject: BIOLOGIA MOLECULAR / NEOPLASIAS Year: 2017 Document type: Article Affiliation country: Taiwán
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Cell Adhesion / Cell Movement / Focal Adhesion Kinase 1 / Dual Specificity Phosphatase 3 Type of study: Prognostic_studies Limits: Animals / Humans Language: En Journal: Oncogene Journal subject: BIOLOGIA MOLECULAR / NEOPLASIAS Year: 2017 Document type: Article Affiliation country: Taiwán