Modulation of VP-16 cytotoxicity by carboplatin and 41.8 degrees C hyperthermia

J Cancer Res Clin Oncol. 2001 Jul;127(7):425-32. doi: 10.1007/s004320000223.

Abstract

Purpose: To study in vitro the effect of carboplatin and/or hyperthermia in relation to etoposide (VP-16) cytotoxicity in L929 cells.

Methodology/results: Cell survival assays demonstrated that the addition of 41.8 degrees C (x60 min) hyperthermia and carboplatin to VP-16 produced an antagonistic effect relative to VP-16 cytotoxicity in L929 cells; administering carboplatin and hyperthermia 24 h before VP-16 reduced this drug resistance; administering carboplatin and hyperthermia 48 h before VP-16, however, produced a supra-additive cytotoxicity. In order to gain insight into the molecular basis for these observations, we investigated the effect of hyperthermia and/or carboplatin on the stress protein GRP78, which is known to affect VP-16 cytotoxicity. Results obtained were consistent with the hypothesis that carboplatin and hyperthermia perturbation of NAD + pools results in down-regulation of GRP78 with subsequent modulation of VP-16 cytotoxicity. To further explicate these results we studied G-361 as a control cell line that had significantly higher pretreatment NAD+ levels, which were not affected by carboplatin and/or hyperthermia. This cell line did not exhibit a down-regulation of GRP78 or modulation of VP-16 cytotoxicity as a function of carboplatin and hyperthermia.

Conclusions: These data taken collectively, demonstrate a sequence effect (regarding the aforementioned antineoplastic agents), and provide a framework for future studies directed at the therapeutic optimization of the sequential application of carboplatin, hyperthermia, and VP-16.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents, Phytogenic / antagonists & inhibitors*
  • Blotting, Western
  • Carboplatin / pharmacology*
  • Cell Survival / drug effects
  • Electrophoresis, Polyacrylamide Gel
  • Endoplasmic Reticulum Chaperone BiP
  • Etoposide / antagonists & inhibitors*
  • Fibrosarcoma / drug therapy*
  • Fibrosarcoma / metabolism
  • Fibrosarcoma / pathology
  • Hyperthermia, Induced*
  • Mice
  • NAD / metabolism
  • Time Factors
  • Tumor Cells, Cultured

Substances

  • Antineoplastic Agents
  • Antineoplastic Agents, Phytogenic
  • Endoplasmic Reticulum Chaperone BiP
  • Hspa5 protein, mouse
  • NAD
  • Etoposide
  • Carboplatin