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Park, Sujin,Yang, Kyung-Min,Park, Yuna,Hong, Eunji,Hong, Chang Pyo,Park, Jinah,Pang, Kyoungwha,Lee, Jihee,Park, Bora,Lee, Siyoung,An, Haein,Kwak, Mi-Kyung,Kim, Junil,Kang, Jin Muk,Kim, Pyunggang,Xiao, Korean Society of Cancer Prevention 2018 Journal of cancer prevention Vol.23 No.1
<P><B>Background</B></P><P>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.</P><P><B>Methods</B></P><P>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.</P><P><B>Results</B></P><P>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, <I>CDH2</I>, <I>SNAI1</I>, and <I>ZEB1</I> in response to TGF-β1 in human pancreatic and prostate cancer cell lines. We identified <I>GADD45B</I>, <I>CTGF</I>, and <I>JUNB</I> genes in the expression profiles associated with cell motility and invasiveness induced by the Smad3-EPSM.</P><P><B>Conclusions</B></P><P>These results suggested that inhibition of Smad3 linker phosphorylation may enhance cell motility and invasiveness by inducing expression of <I>GADD45B</I>, <I>CTGF</I>, and <I>JUNB</I> genes in various cancers.</P>