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The Src family kinase LCK cooperates with oncogenic FLT3/ITD in cellular transformation

Alissa Marhäll1,2, Julhash U Kazi1,2, Lars Rönnstrand3,4,5

  • 1Division of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Medicon Village, Lund, Sweden.

Scientific Reports
|October 25, 2017
PubMed

Insights

The non-receptor tyrosine kinase LCK enhances the function of FLT3-ITD, a mutated receptor tyrosine kinase. LCK promotes cellular transformation and tumor development, highlighting its role in oncogenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Src family kinases, including LCK, are proto-oncogenes regulating cell functions.
  • Receptor tyrosine kinases like FLT3 are crucial in cell signaling and cancer.

Purpose of the Study:

  • To investigate the role of LCK in regulating the function of the type III receptor tyrosine kinase FLT3.
  • To determine if LCK cooperates with oncogenic FLT3 mutations in cellular transformation.

Main Methods:

  • Assessed colony-forming capacity in murine pro-B cells expressing LCK and FLT3 mutants.
  • Utilized mouse xenografts to evaluate tumor development and proliferation (Ki67 staining).
  • Analyzed phosphorylation of key signaling proteins (AKT, ERK1/2, p38, STAT5) via Western blotting.

Main Results:

  • LCK expression significantly enhanced the colony-forming capacity of the FLT3-ITD mutant.
  • Tumor development was accelerated in cells expressing LCK compared to controls.
  • LCK enhanced FLT3-ITD-mediated STAT5 phosphorylation but did not affect AKT, ERK1/2, or p38 phosphorylation.

Conclusions:

  • LCK cooperates with the oncogenic FLT3-ITD mutation in cellular transformation.
  • LCK plays a significant role in promoting the proliferative capacity mediated by FLT3-ITD.
  • These findings suggest LCK as a potential therapeutic target in FLT3-mutated cancers.

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