MiR-198 enhances temozolomide sensitivity in glioblastoma by targeting MGMT

J Neurooncol. 2017 May;133(1):59-68. doi: 10.1007/s11060-017-2425-9. Epub 2017 Apr 19.

Abstract

Glioblastoma is one of the most frequent and aggressive brain tumors. Accumulating evidence indicates that microRNAs are involved in glioma proliferation, invasion and drug resistance. Previous studies showed that miR-198 is downregulated in glioblastoma. However, the function of miR-198 in glioblastoma is still unclear. In this study, we report that miR-198 levels were greatly downregulated in glioblastoma specimens and decreased expression of miR-198 was associated with poor prognosis in patients with glioblastoma. And overexpression of miR-198 increased chemosensitivity to temozolomide in vitro and in vivo. O6-methylguanine-DNA methyltransferase (MGMT) was identified as a direct target of miR-198, and miR-198 overexpression prevented the protein translation of MGMT. Furthermore, overexpression of MGMT restored miR-198-induced chemosensitivity to temozolomide. Moreover, the protein levels of MGMT were upregulated in clinical glioblastoma specimens and inversely correlated with miR-198 levels. In conclusion, our studies revealed that MiR-198 induces chemosensitivity in glioblastoma by targeting MGMT and that miR-198 may be used as a new diagnostic marker and therapeutic target for glioblastoma in the future.

Keywords: Glioblastoma; MGMT; Temozolomide resistance; miR-198.

MeSH terms

  • Adult
  • Aged
  • Animals
  • Antineoplastic Agents, Alkylating / pharmacology
  • Antineoplastic Agents, Alkylating / therapeutic use*
  • Astrocytes / drug effects
  • Astrocytes / metabolism
  • Brain Neoplasms / drug therapy*
  • Brain Neoplasms / metabolism
  • Cell Line, Tumor
  • DNA Modification Methylases / genetics
  • DNA Modification Methylases / metabolism*
  • DNA Repair Enzymes / genetics
  • DNA Repair Enzymes / metabolism*
  • Dacarbazine / analogs & derivatives*
  • Dacarbazine / pharmacology
  • Dacarbazine / therapeutic use
  • Drug Resistance, Neoplasm / physiology
  • Female
  • Glioblastoma / drug therapy*
  • Glioblastoma / metabolism
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Male
  • Mice, Inbred NOD
  • Mice, SCID
  • MicroRNAs / metabolism*
  • Middle Aged
  • Neoplasm Transplantation
  • RNA, Messenger / metabolism
  • Temozolomide
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism*
  • Young Adult

Substances

  • Antineoplastic Agents, Alkylating
  • MIRN198 microRNA, human
  • MicroRNAs
  • RNA, Messenger
  • Tumor Suppressor Proteins
  • Dacarbazine
  • DNA Modification Methylases
  • MGMT protein, human
  • DNA Repair Enzymes
  • Temozolomide