Effects of neoplastic transformation and teniposide (VM26) on protein kinase C isoform expression in rodent fibroblasts

Cancer Lett. 2000 May 29;153(1-2):13-23. doi: 10.1016/s0304-3835(99)00417-6.

Abstract

This study examined changes in protein kinase C (PKC) isoforms in rodent fibroblasts (rat F111 and mouse NIH3T3), transformed by the polyoma virus middle T antigen (mT) and undergoing apoptosis in response to teniposide (VM26). The mT-transformed cells up-regulated PKC delta and down-regulated both PKC epsilon and PKC lambda expression, and were more sensitive to the drug than their non-transformed counterparts. The drug treatment further lowered the expression of PKC epsilon, triggered nuclear translocation of PKC delta and its site-specific proteolysis, consistent with the notion that changes in specific PKC isoforms play a role not only in the neoplastic transformation of fibroblasts, but also in their apoptotic response.

MeSH terms

  • 3T3 Cells
  • Animals
  • Antineoplastic Agents / pharmacology
  • Cell Transformation, Neoplastic*
  • Cells, Cultured
  • Gene Expression
  • Isoenzymes / metabolism*
  • Mice
  • Protein Kinase C / metabolism*
  • Protein Kinase C-delta
  • Protein Kinase C-epsilon
  • Rats
  • Teniposide / pharmacology*

Substances

  • Antineoplastic Agents
  • Isoenzymes
  • Teniposide
  • Prkcd protein, mouse
  • Prkcd protein, rat
  • Prkce protein, mouse
  • Prkce protein, rat
  • Protein Kinase C
  • Protein Kinase C-delta
  • Protein Kinase C-epsilon
  • protein kinase C lambda