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Tumor-suppressive function of mutated gelsolin in ras-transformed cells

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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)
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)

Submitter: 葛巻 暹

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