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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>
( Yuna Park ),( Soohyun Maeng ),( Junsang Oh ),( Gi-ho Sung ),( Sathiyaraj Srinivasan ) 한국균학회 2021 Mycobiology Vol.49 No.5
Three strains, YP416<sup>T</sup>, YP421<sup>T</sup>, and Y422, were isolated from soil samples in Pocheon City, Gyeonggi province, South Korea. The strains belong to two novel yeast species in the genus Mrakia. Molecular phylogenetic analysis showed that the strain YP416<sup>T</sup> was closely related to Mrakia niccombsii. Still, it differed by 9 nucleotide substitutions with no gap (1.51%) in the D1/D2 domain of the LSU rRNA gene and 14 nucleotide substitutions with 7 gaps (2.36%) in the ITS region. The strain YP421<sup>T</sup> differed from the type strain of the most closely related species, Mrakia aquatica, by 5 nucleotide substitutions with no gap (0.81%) in the D1/D2 domain of the LSU rRNA gene and 9 nucleotide substitutions with one gap (1.43%) in the ITS region. The names Mrakia terrae sp. nov. and Mrakia soli sp. nov. are proposed, with type strains YP416<sup>T</sup> (KCTC 27886<sup>T</sup>) and YP421<sup>T</sup> (KCTC 27890<sup>T</sup>), respectively. MycoBank numbers of the strains YP416<sup>T</sup> and YP421<sup>T</sup> are MB 836844 and MB 836847, respectively.
( Yuna Park ),( Dayoung Kim ),( Inho Yang ),( Bomee Choi ),( Jin Woo Lee ),( Seung Namkoong ),( Hyun Jung Koo ),( Sung Ryul Lee ),( Myung Rye Park ),( Hyosun Lim ),( Youn Kyu Kim ),( Sang-jip Nam ),( 한국미생물생명공학회(구 한국산업미생물학회) 2018 Journal of microbiology and biotechnology Vol.28 No.7
The anti-melanogenic effects of the extract of Angelica tenuissima (AT) root and the extract of AT root fermented by Aspergillus oryzae (FAT) were investigated. These effects were determined by measuring the inhibitory activity of AT and FAT on melanin production in B16F10 melanocytes and with in vitro tyrosinase activity assays. The AT extract inhibited melanin production at concentrations above 250 μg/ml, and this inhibitory effect was significantly enhanced by the fermentation process with A. oryzae. HPLC analysis resulted in the isolation of two active compounds from both the AT and FAT extracts. Their chemical structures were identified as decursin and Z-ligustilide through comparison with previously reported NMR data. The decursin and Z-ligustilide contents were increased in the FAT extract and could be responsible for its enhanced inhibitory effects on melanin production and tyrosinase activity compared with that of the AT extract.