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  1. 医歯学総合研究科
  2. 医歯学総合研究科・学術誌論文

CRISPR/Cas9n-Mediated Deletion of the Snail 1Gene (SNAI1) Reveals Its Role in Regulating Cell Morphology, Cell-Cell Interactions, and Gene Expression in Ovarian Cancer (RMG-1) Cells

http://hdl.handle.net/10232/26158
http://hdl.handle.net/10232/26158
f511e29a-c149-4c1c-bb1a-81330366edd4
名前 / ファイル ライセンス アクション
journal.pone.0132260.PDF journal.pone.0132260.PDF (4.9 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2016-03-14
タイトル
タイトル CRISPR/Cas9n-Mediated Deletion of the Snail 1Gene (SNAI1) Reveals Its Role in Regulating Cell Morphology, Cell-Cell Interactions, and Gene Expression in Ovarian Cancer (RMG-1) Cells
タイトル言語 en
著者 原口, みさ子

× 原口, みさ子

WEKO 117628

en Haraguchi, Misako

ja 原口, みさ子

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佐藤, 正宏

× 佐藤, 正宏

WEKO 117629

en Sato, Masahiro

ja 佐藤, 正宏

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小澤, 政之

× 小澤, 政之

WEKO 117630

en Ozawa, Masayuki

ja 小澤, 政之

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言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
要約
内容記述タイプ Other
内容記述 Snail1 is a transcription factor that induces the epithelial to mesenchymal transition (EMT). During EMT, epithelial cells lose their junctions, reorganize their cytoskeletons, and reprogram gene expression. Although Snail1 is a prominent repressor of E-cadherin transcription, its precise roles in each of the phenomena of EMT are not completely understood, particularly in cytoskeletal changes. Previous studies have employed gene knockdown systems to determine the functions of Snail1. However, incomplete protein knockdown is often associated with these systems, which may cause incorrect interpretation of the data. To more precisely evaluate the functions of Snail1, we generated a stable cell line with a targeted ablation of Snail1 (Snail1 KO) by using the CRISPR/Cas9n system. Snail1 KO cells show increased cell–cell adhesion, decreased cell–substrate adhesion and cell migration, changes to their cytoskeletal organization that include few stress fibers and abundant cortical actin, and upregulation of epithelial marker genes such as E-cadherin, occludin, and claudin-1. However, morphological changes were induced by treatment of Snail1 KO cells with TGF-beta. Other transcription factors that induce EMT were also induced by treatment with TGF-beta. The precise deletion of Snail1 by the CRISPR/Cas9n system provides clear evidence that loss of Snail1 causes changes in the actin cytoskeleton, decreases cell–substrate adhesion, and increases cell–cell adhesion. Treatment of RMG1 cells with TGF-beta suggests redundancy among the transcription factors that induce EMT.
内容記述言語 en
収録雑誌名 en : PLOS ONE

巻 10, 号 7, p. e0132260, 発行日 2015-10-07
作成日
日付 2015-10-07
日付タイプ Issued
ISSN
収録物識別子タイプ EISSN
ISSN 19326203
DOI
識別子タイプ DOI
DOI https://doi.org/10.1371/journal.pone.0132260
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
NDC
主題Scheme NDC
主題 464.1
公開者・出版者
出版者 Public Library of Science
出版者言語 en
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