Send to

Choose Destination
See comment in PubMed Commons below
Oncogene. 1993 Sep;8(9):2531-6.

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

Author information

  • 1Laboratory of Molecular Genetics, Hokkaido University School of Medicine, Sapporo, Japan.


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.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Loading ...
    Write to the Help Desk