Down-regulation of EGFR prolonged cell growth of glioma but did not increase the sensitivity to temozolomide

Anticancer Res. 2011 Oct;31(10):3253-7.

Abstract

Background: Malignant glioma is an invasive disease of the central nervous system. One of the factors that regulate growth of these tumors is expression of epidermal growth factor receptor (EGFR) in the cells. This study investigated the effects of down-regulation of EGFR on cell proliferation, cell cycle and cytotoxicity to antineoplastic agent.

Materials and methods: A short hairpin RNA transcription vector targeting EGFR was transfected into KNS42 cells. Growth curve, cell cycle and sensitivity to temozolomide of the cells were assessed.

Results: Transfection inhibited EGFR expression by 50.5%. It prolonged cell doubling time by 25.7%. However, it did not meaningfully alter the cell cycle populations nor increase sensitivity to temozolomide.

Conclusion: Suppressing expression of EGFR inhibited cell proliferation. However, unlike PTEN expression or ROCK1 down-regulation, it did not alter the cell cycle or increase sensitivity to temozolomide.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Cycle / drug effects
  • Cell Death / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Dacarbazine / analogs & derivatives*
  • Dacarbazine / pharmacology
  • Down-Regulation / drug effects*
  • Drug Screening Assays, Antitumor
  • ErbB Receptors / metabolism*
  • Glioma / enzymology
  • Glioma / pathology*
  • Humans
  • RNA, Small Interfering / metabolism
  • Temozolomide
  • Transfection
  • rho-Associated Kinases / metabolism

Substances

  • RNA, Small Interfering
  • Dacarbazine
  • EGFR protein, human
  • ErbB Receptors
  • rho-Associated Kinases
  • Temozolomide