NF‐kB inhibition as a strategy to enhance etoposide‐induced apoptosis in K562 cell line

doi:10.1002/ajh.20732

Paper

NF‐kB inhibition as a strategy to enhance etoposide‐induced apoptosis in K562 cell line

Published Dec 1, 2006 · A. Morotti, D. Cilloni, M. Pautasso

American Journal of Hematology

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Abstract

NF‐kB is a transcription factor that mediates antiapoptotic signals in several cancer cell lines. Here we have demonstrated that the cytotoxic drug, Etoposide, activates NF‐kB in K562, a chronic myeloid leukemia blast crisis cell line. Treatment with the NF‐kB inhibitors MG‐132, Bay11‐7082, and Resveratrol impedes Etoposide‐induced NF‐kB activation, rendering K562 sensitive to Etoposide‐induced apoptosis. Stable expression of mutant form of IkB‐α, which retains NF‐kB inactive in the cytoplasm of cells, confirmed the data obtained with molecular inhibitors. Both inhibitors and stable expression of SR‐IkB are associated with down‐modulation of the antiapoptotic protein Bcl‐xL, suggesting that the survival pathway activated by Etoposide involves NF‐kB‐mediated Bcl‐xL expression. Am. J. Hematol., 2006. © 2006 Wiley‐Liss, Inc.

In Vitro Study

Study Snapshot

Inhibiting NF-kB activity in K562 cells enhances etoposide-induced apoptosis, suggesting a potential strategy for treating chronic myeloid leukemia.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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NF‐kB inhibition as a strategy to enhance etoposide‐induced apoptosis in K562 cell line

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