Dual abrogation of MNK and mTOR: a novel therapeutic approach for the treatment of aggressive cancers

Future Med Chem. 2017 Sep;9(13):1539-1555. doi: 10.4155/fmc-2017-0062. Epub 2017 Aug 25.

Abstract

Targeting the translational machinery has emerged as a promising therapeutic option for cancer treatment. Cancer cells require elevated protein synthesis and exhibit augmented activity to meet the increased metabolic demand. Eukaryotic translation initiation factor 4E is necessary for mRNA translation, its availability and phosphorylation are regulated by the PI3K/AKT/mTOR and MNK1/2 pathways. The phosphorylated form of eIF4E drives the expression of oncogenic proteins including those involved in metastasis. In this article, we will review the role of eIF4E in cancer, its regulation and discuss the benefit of dual inhibition of upstream pathways. The discernible interplay between the MNK and mTOR signaling pathways provides a novel therapeutic opportunity to target aggressive migratory cancers through the development of hybrid molecules.

Keywords: MNK1/2; cancer; cell migration; eIF4E; hybrid drugs; kinase inhibitors; mTOR; resistance; signaling; translation.

Publication types

  • Review

MeSH terms

  • Cell Survival / drug effects
  • Eukaryotic Initiation Factors / metabolism
  • Humans
  • Neoplasms / drug therapy*
  • Neoplasms / pathology
  • Phosphatidylinositol 3-Kinases / metabolism
  • Protein Kinase Inhibitors / chemistry
  • Protein Kinase Inhibitors / therapeutic use*
  • Protein Kinase Inhibitors / toxicity
  • Protein Serine-Threonine Kinases / antagonists & inhibitors
  • Protein Serine-Threonine Kinases / metabolism*
  • Signal Transduction / drug effects
  • TOR Serine-Threonine Kinases / antagonists & inhibitors
  • TOR Serine-Threonine Kinases / metabolism*

Substances

  • Eukaryotic Initiation Factors
  • Protein Kinase Inhibitors
  • MTOR protein, human
  • Protein Serine-Threonine Kinases
  • TOR Serine-Threonine Kinases