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Plectin is a novel regulator for apical extrusion of RasV12-transformed cells

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この文献へのリンクには次のURLを使用してください:http://hdl.handle.net/2115/65782

タイトル: Plectin is a novel regulator for apical extrusion of RasV12-transformed cells
著者: Kadeer, Ailijiang 著作を一覧する
Maruyama, Takeshi 著作を一覧する
Kajita, Mihoko 著作を一覧する
Morita, Tomoko 著作を一覧する
Sasaki, Ayana 著作を一覧する
Ohoka, Atsuko 著作を一覧する
Ishikawa, Susumu 著作を一覧する
Ikegawa, Masaya 著作を一覧する
Shimada, Takashi 著作を一覧する
Fujita, Yasuyuki 著作を一覧する
発行日: 2017年 3月10日
出版者: Nature Publishing Group
誌名: Scientific Reports
巻: 7
開始ページ: 44328
出版社 DOI: 10.1038/srep44328
抄録: Several lines of evidence have revealed that newly emerging transformed cells are often eliminated from the epithelium, though the underlying molecular mechanisms of this cancer preventive phenomenon still remain elusive. In this study, using mammalian cell culture systems we have identified plectin, a versatile cytoskeletal linker protein, as a novel regulator for apical extrusion of RasV12-transformed cells. Plectin is accumulated in RasV12 cells when they are surrounded by normal epithelial cells. Similarly, cytoskeletal proteins tubulin, keratin, and Epithelial Protein Lost In Neoplasm (EPLIN) are also accumulated in the transformed cells surrounded by normal cells. Knockdown or functional disruption of one of these molecules diminishes the accumulation of the others, indicating that the accumulation process of the individual protein mutually depends on each other. Furthermore, plectin-knockdown attenuates caveolin-1 (Cav-1) enrichment and PKA activity in RasV12 cells and profoundly suppresses the apical extrusion. These results indicate that the plectin-microtubules-EPLIN complex positively regulates apical elimination of RasV12-transformed cells from the epithelium in a coordinated fashion. Further development of this study would open a new avenue for cancer preventive medicine.
資料タイプ: article
URI: http://hdl.handle.net/2115/65782
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 藤田 恭之

 

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