Cited by 614Cytokine Signaling Pathways and InteractionsProtein Kinase Regulation and GTPase SignalingNF-κB Signaling Pathways

Stat3 Activation Is Required for Cellular Transformation by v- src

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Bromberg, Jacqueline F., Horvath, Curt M., Besser, Daniel, Lathem, Wyndham W., Darnell, James E.·1998·Molecular and Cellular Biology

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.

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Crossref · 10.1128/mcb.18.5.2553

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  • Activation of STAT3 signaling is a critical component of malignant transformation.

    “Further study revealed that STAT3 activation and specific gene regulation is required for Src-mediated transformation of NIH-3T3 cells, leading to the conclusion that activation of STAT3 signaling is a critical component of malignant transformation.42,43”

    From Critical analysis of the potential for targeting STAT3 in human malignancy (2013) · cites this paper as [42]

    The Discussion (page not available in our copy) reports that activated Stat3 has oncogenic potential and that inhibiting Stat3 reduces v-src transformation in NIH 3T3 cells. The paper concludes that Stat3 activation is necessary for v-src transformation, but does not establish that it is required for malignant transformation generally; it reports no effect on v-ras transformation. (LLM, conf=0.88)

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Research works printed but not linked: 6

  1. [1]1. Ausubel, F. M., R. Brent, R. E. Kingston, D. D. Moore, J. G. Seidman, J. A. Smith, and K. Struhl. 1994. Current protocols in molecular biology. John Wiley and Sons, New York, N.Y.
  2. [4]4. Bromberg, J. F., C. M. Horvath, Z. Wen, R. D. Schreiber, and J. E. Darnell, Jr. 1996. Transcriptionally active Stat1 is required for the antiproliferative effects of both interferon alpha and interferon gamma. Proc. Natl. Acad. Sci. USA 93: 7673-7678.
  3. [22]22. Minami, M., M. Inoue, S. Wei, K. Takeda, M. Matsumoto, T. Kishimoto, and S. Akira. 1996. Stat3 activation is a critical step in gp130-mediated terminal differentiation and growth arrest of a myeloid cell line. Proc. Natl. Acad. Sci. USA 93: 3963-3966.
  4. [30]30. Takeda, K., K. Noguchi, W. Shi, T. Tanaka, M. Matsumoto, N. Yoshida, T. Kishimoto, and S. Akira. 1997. Targeted disruption of the mouse Stat3 gene leads to early embryonic lethality. Proc. Natl. Acad. Sci. USA 94: 3801-3804.
  5. [29]29. Suematsu, S., T. Matsusaka, T. Matsuda, S. Ohno, J. Miyazaki, K. Yamamura, T. Hirano, and T. Kishimoto. 1992. Generation of plasmacytomas with the chromosomal translocation t(12;15) in interleukin 6 transgenic mice. Proc. Natl. Acad. Sci. USA 89: 232-235.
  6. [36]36. Zhang, Q., I. Nowak, E. C. Vonderheid, A. H. Rook, M. E. Kadin, P. C. Nowell, L. M. Shaw, and M. A. Wasik. 1996. Activation of Jak/STAT proteins involved in signal transduction pathway mediated by receptor for interleukin 2 in malignant T lymphocytes derived from cutaneous anaplastic large T-cell lymphoma and Sezary syndrome. Proc. Natl. Acad. Sci. USA 93: 9148-9153.

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Authors
Bromberg, J. F., Horvath, C. M., Besser, D., Lathem, W. W., & Darnell, J. E.
Affiliations
  • Laboratory of Molecular Cell Biology
  • Rockefeller University (US)
Venue
Molecular and Cellular Biology
Published
1998-05
Volume
18
Issue
5
Pages
2553-2558
ISSN
  • 0270-7306 (ISSN-L)
  • 1098-5549
OpenAlex
W2163046152
Cited by
614
References
2
Citations by year
2026: 1 · 2025: 1 · 2024: 4 · 2023: 1 · 2022: 5 · 2021: 5 · 2020: 16 · 2019: 8 · 2018: 9 · 2017: 13 · 2016: 9 · 2015: 16 · 2014: 25 · 2013: 28 · 2012: 24
FWCI
20.39
Type
journal article
Language
en
Open access
Locations
  • Molecular and Cellular Biology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Science Foundation
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
  • National Institutes of Health (5k08ca067950-02)
  • National Cancer Institute (K08 CA67950)
  • National Institute of Allergy and Infectious Diseases (R37AI034420, AI 34420, R01AI032489, AI32489)
Topics
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
STAT3, v-Src, cell transformation, oncogenic transformation, v-ras, cytokine signaling, apoptosis inhibition
MeSH terms
Animals, Cell Survival, Cell Transformation, Neoplastic, DNA-Binding Proteins, Stem Cells, Trans-Activators, Oncogene Protein pp60(v-src), Gene Expression Regulation, Neoplastic, 3T3 Cells, STAT3 Transcription Factor, Mice

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