Fludarabine Nucleoside Modulates Nuclear “Survival and Death” Proteins in Resistant Chronic Lymphocytic Leukemia Cells

Silke Henrich, Swetlana Mactier, Giles Best, Stephen P. Mulligan, Ben Crossett, Richard Ian Christopherson

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)

Abstract

The nuclear mechanisms by which fludarabine nucleoside (F-ara-A) induces apoptosis have been investigated in human MEC1 cells derived from B-cell chronic lymphocytic leukemia. Upon treatment of cells with F-ara-A (100 μM, 72 hours), 15 nuclear proteins changed in abundance by more than 2-fold. Nuclear proteins up-regulated included calmodulin (4.3-fold), prohibitin (3.9-fold), β-actin variant (3.7-fold), and structure-specific recognition protein 1 (3.7-fold); those downregulated included 60S ribosomal protein P2B (0.12-fold), fumarate hydratase (0.19-fold), splicing factor arginine/serine-rich 3 (0.35-fold), and replication protein A2 (0.42-fold). These changes in the levels of specific proteins promote survival or apoptosis; because the end result is apoptosis of MEC1 cells, apoptotic effects predominate.

Original languageEnglish
Pages (from-to)1181-1189
Number of pages9
JournalNucleosides, Nucleotides and Nucleic Acids
Volume30
Issue number12
DOIs
Publication statusPublished - Dec 2011
Externally publishedYes

Keywords

  • Apoptosis
  • Chronic lymphocytic leukemia
  • DIGE
  • Fludarabine
  • Nuclear proteome

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