Anti-miR-155 oligonucleotide enhances chemosensitivity of U251 cell to taxol by inducing apoptosis

Cell Biol Int. 2012 Jul;36(7):653-9. doi: 10.1042/CBI20100918.

Abstract

The oncogene, microRNA-155, is significantly elevated in GBM (glioblastoma multiforme), regulating multiple genes associated with cancer cell proliferation, apoptosis and invasiveness. Thus, miR-155 can theoretically become a target for enhancement of the chemotherapy in cancer. Down-regulating miR-155 to enhance the effect of taxol has not been studied in human GBM. Human GBM U251 cells were treated with taxol and the miR-155 inhibitor alone or in combination. IC50 values were dramatically decreased in cells treated with miR-155 inhibitor combined with taxol, to a greater extent than those treated with taxol alone. Furthermore, the miR-155 inhibitor significantly enhanced apoptosis in U251 cells. The data suggest that miR-155 blockage increased the chemosensitivity to taxol in GBM cells, making combined treatment an effective therapeutic strategy for controlling the growth by inhibiting EAG1 expression.

MeSH terms

  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Apoptosis / drug effects*
  • Cell Line, Tumor
  • Down-Regulation / drug effects
  • Ether-A-Go-Go Potassium Channels / genetics
  • Ether-A-Go-Go Potassium Channels / metabolism
  • Glioblastoma / metabolism
  • Glioblastoma / pathology
  • Humans
  • MicroRNAs / antagonists & inhibitors*
  • MicroRNAs / metabolism
  • Oligonucleotides, Antisense / metabolism*
  • Paclitaxel / pharmacology*

Substances

  • Antineoplastic Agents, Phytogenic
  • Ether-A-Go-Go Potassium Channels
  • KCNH1 protein, human
  • MIRN155 microRNA, human
  • MicroRNAs
  • Oligonucleotides, Antisense
  • Paclitaxel