@article{oai:u-ryukyu.repo.nii.ac.jp:02017767,
 author = {Ulziikhishig, Enkhbaatar and Bayarjargal, Maitsetseg and Nonaka, Kimiko and Oshiro, Minoru and Kariya, Ken-ichi},
 issue = {3･4},
 journal = {琉球医学会誌 = Ryukyu Medical Journal},
 note = {Purpose: Traf2- and Nck-interacting kinase (TNIK) is one of the effector kinases of the Ras-like GTPase Rap2, and belongs to the STE20 group of mitogen-activated protein kinase kinase kinase kinases (MAP4Ks). The purpose of this study was to explore the roles of TNIK in the phenotype of cancer cells. Results: Derivatives of a cutaneous squamous cell carcinoma (SCC) cell line, Pam212, in which expression of hemagglutinin-tagged TNIK (HA-TNIK) can be induced by modulating the concentration of a tetracycline derivative in culture medium were established by using a retrovirus-mediated gene transduction system. Morphological analyses revealed that HA-TNIK regulated intercellular adhesion and epithelial cell shape. A strong induction of HA-TNIK disrupted intercellular adhesion and abolished the epithelial cell shape. Moderately induced HA-TNIK co-localized with E-cadherin, a principal component of intercellular adherens junctions (AJs), and facilitated cellular detachment during hepatocyte growth factor-induced cell scattering and wound-healing cell migration assays. Moderately induced HA-TNIK also retarded Ca^<2_+>-dependent re-assembly of AJs that had been pre-disassembled by transient depletion of Ca^<2_+> in culture medium. Conclusion: These results complement our preceding work using a proteomic approach (Kuninaka et al. "Proteomic changes in a squamous cell carcinoma cell line induced by an effector kinase of a small G protein Rap2" Ryukyu Med. J. 26: 135-145, 2007) on roles of TNIK in SCC cells., 論文},
 pages = {89--94},
 title = {[原著]Phenotypic changes in a squamous cell carcinoma cell line induced by an effector kinase of a small G protein Rap2},
 volume = {32}
}