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PMID: 9566875 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Stat3 activation is required for cellular transformation by v-src.

Molecular and cellular biology ·Vol. 18 ·No. 5 ·1998-05-00 ·Pages 2553-8

Bromberg JF, Horvath CM, Besser D, Lathem WW, Darnell JE

Abstract

Stat3 activation has been associated with cytokine-induced proliferation, anti-apoptosis, and transformation. Constitutively activated Stat3 has been found in many human tumors as well as v-abl- and v-src-transformed cell lines. Because of these correlations, we examined directly the relationship of activated Stat3 to cellular transformation and found that wild-type Stat3 enhances the transforming potential of v-src while three dominant negative Stat3 mutants inhibit v-src transformation. Stat3 wild-type or mutant proteins did not affect v-ras transformation. We conclude that Stat3 has a necessary role in v-src transformation.

MeSH Terms
3T3 Cells Animals Cell Survival Cell Transformation, Neoplastic DNA-Binding Proteins/genetics,metabolism Gene Expression Regulation, Neoplastic Mice Oncogene Protein pp60(v-src)/metabolism STAT3 Transcription Factor Stem Cells Trans-Activators/genetics,metabolism
Chemicals
DNA-Binding Proteins STAT3 Transcription Factor Stat3 protein, mouse Trans-Activators Oncogene Protein pp60(v-src)
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Bromberg J F
Laboratory of Molecular Cell Biology, The Rockefeller University, New York, New York 10021-6399, USA.
Horvath C M
Besser D
Lathem W W
Darnell J E
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Article Info
Journal
Molecular and cellular biology
Abbr.
Mol Cell Biol
ISSN
0270-7306
DOI
10.1128/MCB.18.5.2553
Published
1998-05-00
Pages
2553-8
Language
English
Region
United States
NLM ID
8109087
PMCID
PMC110635
Subset
IM
Grants
NIAID NIH HHS · AI34420 · United States
NIAID NIH HHS · AI32489 · United States
NCI NIH HHS · K08 CA67950 · United States
External Links
PubMed source DOI: 10.1128/MCB.18.5.2553 PMC Full Text View journal details
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