Dual Inhibition of PDK1 and Aurora Kinase A: An Effective Strategy to Induce Differentiation and Apoptosis of Human Glioblastoma Multiforme Stem Cells

ACS Chem Neurosci. 2017 Jan 18;8(1):100-114. doi: 10.1021/acschemneuro.6b00251. Epub 2016 Nov 10.

Abstract

The poor prognosis of glioblastoma multiforme (GBM) is mainly attributed to drug resistance mechanisms and to the existence of a subpopulation of glioma stem cells (GSCs). Multitarget compounds able to both affect different deregulated pathways and the GSC subpopulation could escape tumor resistance and, most importantly, eradicate the stem cell reservoir. In this respect, the simultaneous inhibition of phosphoinositide-dependent kinase-1 (PDK1) and aurora kinase A (AurA), each one playing a pivotal role in cellular survival/migration/differentiation, could represent an innovative strategy to overcome GBM resistance and recurrence. Herein, the cross-talk between these pathways was investigated, using the single-target reference compounds MP7 (PDK1 inhibitor) and Alisertib (AurA inhibitor). Furthermore, a new ligand, SA16, was identified for its ability to inhibit the PDK1 and the AurA pathways at once, thus proving to be a useful tool for the simultaneous inhibition of the two kinases. SA16 blocked GBM cell proliferation, reduced tumor invasiveness, and triggered cellular apoptosis. Most importantly, the AurA/PDK1 blocker showed an increased efficacy against GSCs, inducing their differentiation and apoptosis. To the best of our knowledge, this is the first report on combined targeting of PDK1 and AurA. This drug represents an attractive multitarget lead scaffold for the development of new potential treatments for GBM and GSCs.

Keywords: Aurora Kinase A; Glioblastoma multiforme; glioma stem cells; multitarget compounds; phosphoinositide-dependent kinase-1.

MeSH terms

  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Aurora Kinase A / genetics
  • Aurora Kinase A / metabolism*
  • Brain Neoplasms / pathology
  • Cell Differentiation / drug effects
  • Cell Differentiation / physiology*
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Dose-Response Relationship, Drug
  • Drug Synergism
  • Enzyme Inhibitors / chemical synthesis
  • Enzyme Inhibitors / chemistry
  • Enzyme Inhibitors / pharmacology
  • Gene Expression Regulation, Neoplastic / drug effects
  • Glioblastoma / pathology
  • Humans
  • Neoplastic Stem Cells / drug effects
  • Neoplastic Stem Cells / enzymology*
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism
  • Protein Binding / drug effects
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • Pyruvate Dehydrogenase Acetyl-Transferring Kinase
  • RNA, Messenger / metabolism
  • Stem Cells / drug effects
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / enzymology
  • Time Factors

Substances

  • Enzyme Inhibitors
  • Nerve Tissue Proteins
  • PDK1 protein, human
  • Pyruvate Dehydrogenase Acetyl-Transferring Kinase
  • RNA, Messenger
  • Aurora Kinase A
  • Protein Serine-Threonine Kinases