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KMID : 1140220180230010001
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대한암예방학회지
2018 Volume.23 No. 1 p.1 ~ p.9
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Identification of Epithelial-Mesenchymal Transition-related Target Genes Induced by the Mutation of Smad3 Linker Phosphorylation
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Park Su-Jin
Yang Kyung-Min
Park Yu-Na
Hong Eun-Ji
Hong Chang-Pyo
Park Jin-Ah
Pang Kyoung-Wha
Lee Ji-Hee
Park Bo-Ra
Lee Si-Young
An Hae-In
Kwak Mi-Kyung
Kim Jun-Il
Kang Jin-Muk
Kim Pyung-Gang
Xiao Yang
Nie Guangjun
Ooshima Akira
Kim Seong-Jin
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Abstract
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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.
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KEYWORD
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Smad3, Epithelial-mesenchymal transition, Pancreatic cancer, Prostate cancer, RNA sequence analysis
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