Alternative Titleビメンチン中間径フィラメントとプレクチンによる浸潤突起の足場形成は癌転移のための浸潤および血管外脱出過程を促進する
ビメンチン チュウカンケイ フィラメント ト プレクチン ニヨル シンジュン トッキ ノ アシバ ケイセイ ワ ガン テンイ ノタメノ シンジュン オヨビ ケッカンガイ ダッシュツ カテイ オ ソクシンスル
Periodical titleEuropean Journal of Cell Biology
Note (General)type:Thesis
To investigate the molecular mechanisms of cancer metastasis, we have isolated a high-metastatic bladder cancer cell subpopulation from a low-metastatic cell line by using an in vivo selection system. Cells in the subpopulation showed a high ability to form invadopodia, the filamentous actin (F-actin)-based membrane protrusions that play an essential role in cancer cell invasion. Analysis of the gene expression profile revealed that the expression of an intermediate filament (IF) protein, vimentin and a cytoskeletal linker protein, plectin was up-regulated in the high-metastatic subpopulation compared with the low metastatic cell line. Here we report a novel role of vimentin IF and plectin in metastasis. In invasive bladder cancer cells, the vimentin IF-plectin-invadopodia F-actin link was formed. Disruption of this link severely impaired invadopodia formation, reducing the capacities of extracellular matrix degradation, transendothelial migration and metastasis. In addition, the vimentin assembly into the filaments was required for invadopodia formation. Our results suggest that plectin anchoring invadopodia to vimentin IF scaffolds and stabilizes invadopodia, which is a critical molecular process for cancer cell invasion and extravasation for metastasis.
掲載誌本文リンク:http://www.sciencedirect.com/science/article/pii/S017193351400048X
identifier:European Journal of Cell Biology, 93(4), 2014, p.157-169
DOIinfo:doi/10.1016/j.ejcb.2014.03.002
Collection (particular)国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
Date Accepted (W3CDTF)2015-02-03T05:25:05+09:00
Data Provider (Database)国立国会図書館 : 国立国会図書館デジタルコレクション