Proliferation of C6 glioma cells is blunted by the increase in gap junction communication caused by tolbutamide

FEBS Lett. 2001 Dec 7;509(2):202-6. doi: 10.1016/s0014-5793(01)03181-7.

Abstract

We have previously reported that tolbutamide prevents the inhibition of gap junction communication in astrocytes. Here, we show that tolbutamide increases gap junction communication and connexin 43 expression in poorly coupled C6 glioma cells. The increase in communication is concurrent with the inhibition of the rate of proliferation due to a block of the progression of C6 glioma cells through the S phase of the cell cycle. The effects of tolbutamide were quantitatively similar to that found after the elevation of intracellular cAMP. Furthermore, the effects of tolbutamide and cAMP were additive. The possible beneficial effect of tolbutamide on gene therapy for gliomas is discussed.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Communication / drug effects
  • Cell Division / drug effects
  • Cell Membrane Permeability / drug effects
  • Connexin 43 / biosynthesis
  • Cyclic AMP / metabolism
  • Gap Junctions / drug effects*
  • Glioma / drug therapy*
  • Rats
  • S Phase / drug effects
  • Tolbutamide / pharmacology*

Substances

  • Connexin 43
  • Tolbutamide
  • Cyclic AMP