Role of GST P1-1 in mediating the effect of etoposide on human neuroblastoma cell line SH-SY5Y

S. Bernardini, L. Bellincampi, S. Ballerini, M. Ranalli, A. Pastore, C. Cortese, G. Federici

Research output: Contribution to journalArticlepeer-review

Abstract

The oxidative stress could have a dual action on glutathione S-transferase (GST) P1-1 metabolism: transcriptional induction and/or polymerization. The former should represent a form of adaptation to oxidative stress and contribute to protect the cell, the latter one should activate apoptosis via c-Jun N-terminal kinase (JNK). We studied the effect of etoposide on human neuroblastoma cell line SH-SY5Y and on an etoposide-resistant clone to investigate whether a pleiotropic effect of etoposide on the redox status of the cell exists which is able to interfere with apoptosis through the GST P1-1 system. Etoposide treatment was able to induce GST P1-1 polymerization and activation of apoptosis. The data obtained from our etoposide-resistant clone and the possibility to reverse the sensitive phenotype to a resistant one by means of hexyl-glutathione preincubation, seem to suggest that cellular levels of glutathione have a key role in protecting GST P1-1 by oxidation and consequently the cell's decision between life and death.

Original languageEnglish
Pages (from-to)340-347
Number of pages8
JournalJournal of Cellular Biochemistry
Volume86
Issue number2
DOIs
Publication statusPublished - 2002

Keywords

  • Apoptosis
  • Drug resistance
  • Etoposide
  • Glutathione
  • Glutathione transferase P1-1

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

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