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Dual targeting of eIF4E by blocking MNK and mTOR pathways in leukemia

Ewa M Kosciuczuk1, Diana Saleiro2, Leonidas C Platanias1

  • 1Robert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Medicine, Jesse Brown Veterans Affairs Medical Center, Chicago, IL 60612, USA.

Cytokine
|April 21, 2016
PubMed

Insights

Dysregulated mRNA translation, driven by eukaryotic translation initiation factor 4E (eIF4E), fuels leukemia. Targeting MAPK and mTOR pathways controlling eIF4E offers a potential strategy to inhibit leukemic cell survival and proliferation.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Biochemistry

Background:

  • Aberrant mRNA translation promotes leukemic clone expansion and survival.
  • Eukaryotic translation initiation factor 4E (eIF4E) is crucial for translation initiation.
  • Mitogen-activated protein kinase (MAPK) and mammalian target of rapamycin (mTOR) pathways regulate eIF4E activity.

Purpose of the Study:

  • To investigate the role of MAPK and mTOR pathways in regulating eIF4E in leukemia.
  • To explore the potential of targeting these pathways for leukemia treatment.

Main Methods:

  • Analysis of mRNA translation regulation in leukemic cells.
  • Investigating the phosphorylation status of eIF4E and its inhibitor 4E-BP1.
  • Examining the activity of MAPK, mTOR, and Mnk pathways.

Main Results:

  • Dysregulated mRNA translation and eIF4E activity are observed in leukemia.
  • MAPK and mTOR pathways are abnormally activated in leukemia cells.
  • Mitogen-activated protein kinase interacting protein kinases (Mnks) phosphorylate eIF4E, while mTOR deactivates 4E-BP1.

Conclusions:

  • Abnormal activation of MAPK and mTOR pathways contributes to leukemia pathogenesis by controlling oncogenic protein expression.
  • Targeting these translation regulatory pathways presents a promising therapeutic strategy for leukemia.
Keywords:
Acute myeloid leukemiaMNKTranslation initiationeIF4EmTOR

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