The Src tyrosine kinase Hck is required for Tel-Abl- but not for Tel-Jak2-induced cell transformation

C. Pecquet, R. Nyga, V. Penard-Lacronique, T. E. Smithgall, H. Murakami, A. Régnier, K. Lassoued, F. Gouilleux

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Abstract

Tel-Abl and Tel-Jak2 are fusion proteins associated with human haematologic neoplasms. They possess constitutive tyrosine kinase activity and activate common downstream signalling pathways like Stat-5, PI3-K/Akt, Ras/MapK and NF-κB. In this study, we showed the specific requirement of Src family members for the Tel-Abl-mediated cell growth, activation of Stat5, PI3-K/Akt and Ras/MapK while dispensable for Tel-Jak2. Hck was found strongly phosphorylated in Tel-Abl-expressing Ba/F3 cells and sensitive to imatinib mesylate treatment, providing evidence that Hck is a target of Tel-Abl tyrosine kinase activity. Overexpression of a kinase dead form of Hck inhibits the proliferation of Ba/F3 cells expressing Tel-Abl as the phosphorylation of Akt and Erk1/2. These results argue for an important role of Hck in Tel-Abl oncogenic signalling.

Original languageEnglish
Pages (from-to)1577-1585
Number of pages9
JournalOncogene
Volume26
Issue number11
DOIs
Publication statusPublished - Mar 8 2007

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Keywords

  • Hck
  • Oncogenes
  • Signal transduction
  • Src kinases
  • Tel-Abl
  • Tel-Jak2

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

Cite this

Pecquet, C., Nyga, R., Penard-Lacronique, V., Smithgall, T. E., Murakami, H., Régnier, A., Lassoued, K., & Gouilleux, F. (2007). The Src tyrosine kinase Hck is required for Tel-Abl- but not for Tel-Jak2-induced cell transformation. Oncogene, 26(11), 1577-1585. https://doi.org/10.1038/sj.onc.1209949