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Journal of cancer prevention v.23 no.1, 2018년, pp.1 - 9  

Identification of Epithelial-Mesenchymal Transition-related Target Genes Induced by the Mutation of Smad3 Linker Phosphorylation

Park, Sujin    (Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Suwon, Korea  ); Yang, Kyung-Min    (Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Suwon, Korea  ); Park, Yuna    (Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Suwon, Korea  ); Hong, Eunji    (Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Suwon, Korea  ); Hong, Chang Pyo    (Theragen Etex Bio Institute, Suwon, Korea  ); Park, Jinah    (Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Suwon, Korea  ); Pang, Kyoungwha    (Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Suwon, Korea  ); Lee, Jihee    (Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Suwon, Korea  ); Park, Bora    (Precision Medicine Research Center, Advanced Institutes of Con  ); Lee, Siyoung   An, Haein   Kwak, Mi-Kyung   Kim, Junil   Kang, Jin Muk   Kim, Pyunggang   Xiao, Yang   Nie, Guangjun   Ooshima, Akira   Kim, Seong-Jin  
  • 초록

    Background Smad3 linker phosphorylation plays essential roles in tumor progression and metastasis. We have previously reported that the mutation of Smad3 linker phosphorylation sites (Smad3-Erk/Pro-directed kinase site mutant constructs [EPSM]) markedly reduced the tumor progression while increasing the lung metastasis in breast cancer. Methods We performed high-throughput RNA-Sequencing of the human prostate cancer cell lines infected with adenoviral Smad3-EPSM to identify the genes regulated by Smad3-EPSM. Results In this study, we identified genes which are differentially regulated in the presence of Smad3-EPSM. We first confirmed that Smad3-EPSM strongly enhanced a capability of cell motility and invasiveness as well as the expression of epithelial-mesenchymal transition marker genes, CDH2 , SNAI1 , and ZEB1 in response to TGF-β1 in human pancreatic and prostate cancer cell lines. We identified GADD45B , CTGF , and JUNB genes in the expression profiles associated with cell motility and invasiveness induced by the Smad3-EPSM. Conclusions These results suggested that inhibition of Smad3 linker phosphorylation may enhance cell motility and invasiveness by inducing expression of GADD45B , CTGF , and JUNB genes in various cancers.


  • 주제어

    Smad3 .   Epithelial-mesenchymal transition .   Pancreatic cancer .   Prostate cancer .   RNA sequence analysis.  

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