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Different growth and metastatic phenotypes associated with a cell-intrinsic change of Met in metastatic melanoma

フォーマット:
論文
責任表示:
Adachi, Eri ; Sakai, Katsuya ; Nishiuchi, Takumi ; Imamura, Ryu ; Sato, Hiroki ; Matsumoto, Kunio
言語:
英語
出版情報:
Impact Journals LLC, 2016-01-01
著者名:
Adachi, Eri
Sakai, Katsuya
Nishiuchi, Takumi
Imamura, Ryu
Sato, Hiroki
Matsumoto, Kunio
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掲載情報:
Oncotarget
ISSN:
1949-2553  CiNii Research  Webcat Plus  JAIRO
巻:
7
通号:
43
開始ページ:
70779
終了ページ:
70793
バージョン:
publisher
概要:
A dynamic phenotypic change contributes to the metastatic progression and drug resistance in malignant melanoma. Nevertheless, mechanisms for a phenotypic change have remained to be addressed. Here, we show that Met receptor expression changes in a cell-autonomous manner and can distinguish phenotypical differences in growth, as well as in metastatic and drug-resistant characteristics. In metastatic melanoma, the cells are composed of Met-low and Met-high populations. Met-low populations have stem-like gene expression profiles, are resistant to chemotherapeutic agents, and have shown abundant angiogenesis and rapid tumor growth in subcutaneous inoculation. Met-high populations have a differentiated phenotype, are relatively resistant to B-RAF inhibitor, and are highly metastatic to the lungs. Met plays a definitive role in lung metastasis because the lung metastasis of Met-high cells requires Met, and treatment of mice with the Met-containing exosomes from Methigh cells facilitates lung metastasis by Met-low cells. Clonal cell fate analysis showed the hierarchical phenotypical changes from Met-low to Met-high populations. Met-low cells either showed self-renewal or changed into Met-high cells, whereas Met-high cells remained Met-high. Clonal transition from Met-low to Met-high cells accompanied changes in the gene expression profile, in tumor growth, and in metastasis that were similar to those in Met-high cells. These findings indicate that malignant melanoma has the ability to undergo phenotypic change by a cell-intrinsic/autonomous mechanism that can be characterized by Met expression. 続きを見る
URL:
http://hdl.handle.net/2297/46523
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