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ADAM-like Decysin-1 (ADAMDEC1) is a positive regulator of Epithelial Defense Against Cancer (EDAC) that promotes apical extrusion of RasV12-transformed cells
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| Title: | ADAM-like Decysin-1 (ADAMDEC1) is a positive regulator of Epithelial Defense Against Cancer (EDAC) that promotes apical extrusion of RasV12-transformed cells |
| Authors: | Yako, Yuta Browse this author | | Hayashi, Takashi Browse this author | | Takeuchi, Yasuto Browse this author →KAKEN DB | | Ishibashi, Kojiro Browse this author | | Kasai, Nobuhiro Browse this author | | Sato, Nanami Browse this author | | Kuromiya, Keisuke Browse this author | | Ishikawa, Susumu Browse this author | | Fujita, Yasuyuki Browse this author →KAKEN DB |
| Issue Date: | 25-Jun-2018 |
| Publisher: | Nature Publishing Group |
| Journal Title: | Scientific reports |
| Volume: | 8 |
| Start Page: | 9639 |
| Publisher DOI: | 10.1038/s41598-018-27469-z |
| Abstract: | Recent studies have revealed that newly emerging transformed cells are often eliminated from epithelia via cell competition with the surrounding normal epithelial cells. However, it remains unknown whether and how soluble factors are involved in this cancer preventive phenomenon. By performing stable isotope labeling with amino acids in cell culture (SILAC)-based quantitative mass spectrometric analyses, we have identified ADAM-like Decysin-1(ADAMDEC1) as a soluble protein whose expression is upregulated in the mix culture of normal and RasV12-transformed epithelial cells. Expression of ADAMDEC1 is elevated in normal epithelial cells co-cultured with RasV12 cells. Knockdown of ADAMDEC1 in the surrounding normal cells substantially suppresses apical extrusion of RasV12 cells, suggesting that ADAMDEC1 secreted by normal cells positively regulate the elimination of the neighboring transformed cells. In addition, we show that the metalloproteinase activity of ADAMDEC1 is dispensable for the regulation of apical extrusion. Furthermore, ADAMDEC1 facilitates the accumulation of filamin, a crucial regulator of Epithelial Defense Against Cancer (EDAC), in normal cells at the interface with RasV12 cells. This is the first report demonstrating that an epithelial intrinsic soluble factor is involved in cell competition in mammals. |
| Rights: | http://creativecommons.org/licenses/by/4.0/ |
| Type: | article |
| URI: | http://hdl.handle.net/2115/71367 |
| Appears in Collections: | 遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 藤田 恭之
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