Nothing Special   »   [go: up one dir, main page]

A Promising Way to Overcome Temozolomide Resistance through Inhibition of Protein Neddylation in Glioblastoma Cell Lines

Int J Mol Sci. 2023 Apr 27;24(9):7929. doi: 10.3390/ijms24097929.

Abstract

There is no effective therapy for the lately increased incidence of glioblastoma multiforme (GBM)-the most common primary brain tumor characterized by a high degree of invasiveness and genetic heterogeneity. Currently, DNA alkylating agent temozolomide (TMZ) is the standard chemotherapy. Nevertheless, TMZ resistance is a major problem in the treatment of GBM due to numerous molecular mechanisms related to DNA damage repair, epigenetic alterations, cellular drug efflux, apoptosis-autophagy, and overactive protein neddylation. Low molecular weight inhibitors of NEDD8-activating enzyme (NAE), such as MLN4924, attenuate protein neddylation and present a promising low-toxicity anticancer agent. The aim of our study was to find an effective combination treatment with TMZ and MLN4924 in our TMZ-resistant GBM cell lines and study the effect of these combination treatments on different protein expressions such as O6-methylguanine methyltransferase (MGMT) and p53. The combination treatment successfully decreased cell viability and sensitized TMZ-resistant cells to TMZ, foreshadowing a new treatment strategy for GBM.

Keywords: combination treatment; glioblastoma multiforme; neddylation; temozolomide.

MeSH terms

  • Antineoplastic Agents, Alkylating / pharmacology
  • Antineoplastic Agents, Alkylating / therapeutic use
  • Brain Neoplasms* / pathology
  • Cell Line, Tumor
  • DNA Modification Methylases / genetics
  • DNA Repair Enzymes / genetics
  • Drug Resistance, Neoplasm
  • Glioblastoma* / metabolism
  • Humans
  • Temozolomide / pharmacology
  • Temozolomide / therapeutic use

Substances

  • Temozolomide
  • pevonedistat
  • Antineoplastic Agents, Alkylating
  • DNA Modification Methylases
  • DNA Repair Enzymes