Resistance of NIH3T3 cells to v-fes transformation induced by a dominant negative H-ras mutant.

Abstract:

:NIH3T3 cells carrying a dominant negative H-ras mutant 116Y acquired resistance to transformation by some PTK oncogenes, i.e., v-fes, v-abl, and v-fms, but were sensitive to viral ras and serine threonine kinase oncogenes, v-raf and v-mos. One clone, designated 1-20, infected with v-fes (1-20 fes) exhibited flat morphology and anchorage-dependent cell growth, as did noninfected 1-20 cells. The 1-20 fes cells expressed v-fes oncogene and produced transforming viruses, although these levels were much lower than those in NIH3T3 cells infected with v-fes (NIH3T3 fes). v-fes mRNAs in NIH3T3 fes cells rapidly increased after infection, while accumulation of the v-fes transcripts in 1-20 fes cells was significantly prolonged. Total tyrosine phosphorylation in both NIH3T3 fes and 1-20 fes cells was correlated with the amounts of pp110v-fes. A few proteins were phosphorylated only in NIH3T3 fes but not in 1-20 fes cells. These results suggest that the cellular ras is involved in a signaling pathway from pp110v-fes and this signal stimulates v-fes expression. Inhibition of the ras function may down-regulate this pathway and result in resistance to transformation by v-fes.

journal_name

Exp Cell Res

authors

Ogiso Y,Yokoyama T,Watari H,Shih TY,Kuzumaki N

doi

10.1006/excr.1993.1263

subject

Has Abstract

pub_date

1993-10-01 00:00:00

pages

415-21

issue

2

eissn

0014-4827

issn

1090-2422

pii

S0014-4827(83)71263-2

journal_volume

208

pub_type

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