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Tumor-suppressive function of mutated gelsolin in ras-transformed cells
| Title: | Tumor-suppressive function of mutated gelsolin in ras-transformed cells |
| Authors: | Mullauer, Leonhard Browse this author | | Fujita, Hisakazu Browse this author | | Ishizaki, Akira Browse this author | | Kuzumaki, Noboru4 Browse this author |
| Authors(alt): | 葛巻, 暹4 |
| Issue Date: | Sep-1993 |
| Publisher: | Nature Publishing Group |
| Journal Title: | Oncogene |
| Volume: | 8 |
| Issue: | 9 |
| Start Page: | 2531 |
| End Page: | 2536 |
| Abstract: | The flat revertant R1, isolated from human activated Ha-ras oncogene-transformed NIH3T3 fibroblasts (EJ-NIH3T3), expresses a variant form of the actin-regulatory protein gelsolin (p92-5.7). We have cloned CDNAS encoding p92-5.7 and identified as the cause of the expression of p92-5.7 a point mutation in codon 321, which results in an amino acid change from proline to histidine. In order to understand the role of p92-5.7 in reversion of ras-transformed cells, CDNAS encoding p92-5.7 or human authentic gelsolin as a control were transfected into EJ-NIH3T3 cells. All the transfectants that produced p92-5.7 and one of three transfectants that produced human authentic gelsolin either lost or reduced tumorigenicity in syngeneic mice. These results demonstrate that mutated gelsolin can suppress a ras tumor and suggest that authentic gelsolin, if expressed at increased levels, may have a similar suppressive potential. Our data propose an important role for gelsolin in cellular signal transduction pathways that involve the mammalian ras proto-oncogene. |
| Type: | article (author version) |
| URI: | http://www.nature.com/onc/index.html | | http://hdl.handle.net/2115/762 |
| 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: 葛巻 暹
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