Newcastle disease virus enhances the growth-inhibiting and proapoptotic effects of temozolomide on glioblastoma cells in vitro and in vivo

Sci Rep. 2018 Jul 31;8(1):11470. doi: 10.1038/s41598-018-29929-y.

Abstract

Glioblastoma (GBM) is the most serious and most common brain tumor in humans. Despite recent advances in the diagnosis of GBM and the development of new treatments, the prognosis of patients has not improved. Multidrug resistance, particularly resistance to temozolomide (TMZ), is a challenge in combating glioma, and more effective therapies are needed. Complementary treatment with the LaSota strain of the naturally oncolytic Newcastle disease virus (NDV-LaSota) is an innovation. In our experiments, the combination therapy of NDV-LaSota and temozolomide (TMZ) was more effective than either treatment alone in inducing apoptosis in glioma cells. NDV can function as a tumor cell selective approach to inhibit AKT and activate AMPK. Consequently, mTOR, 4EBP1 and S6K were also suppressed. The combination therapy of NDV and TMZ also significantly extended survival in a rat xenograft tumor model. In conclusion, NDV suppress AKT signaling and enhances antitumor effects of TMZ. Our study provides one of the theoretical basis for the use of a combined therapy of TMZ and NDV, which could benefit GBM patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • AMP-Activated Protein Kinases / metabolism
  • Animals
  • Antineoplastic Agents, Alkylating / pharmacology*
  • Apoptosis / drug effects*
  • Brain Neoplasms / drug therapy*
  • Brain Neoplasms / virology
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • Chickens
  • Drug Resistance, Multiple / drug effects
  • Drug Resistance, Neoplasm / drug effects
  • Glioblastoma / drug therapy*
  • Glioblastoma / virology
  • Glioma / drug therapy
  • Glioma / virology
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Male
  • Newcastle disease virus / pathogenicity*
  • Oncolytic Viruses / pathogenicity
  • Proto-Oncogene Proteins c-akt / metabolism
  • Rats
  • Rats, Wistar
  • Signal Transduction / drug effects
  • TOR Serine-Threonine Kinases / metabolism
  • Temozolomide / pharmacology*
  • Xenograft Model Antitumor Assays / methods

Substances

  • Antineoplastic Agents, Alkylating
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases
  • AMP-Activated Protein Kinases
  • Temozolomide