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Updated: Apr 28, 2026

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
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Molecular mechanisms of converting K562/DNR cellular drug-resistance by bortezomib

Y-C Li1, H-H Wang, A-J Liao

  • 1Department of Hematology, Shengjing Hospital, China Medical University, Shenyang, China. ycchina27@163.com.

European Review for Medical and Pharmacological Sciences
|June 6, 2014
PubMed
Abstract

Insights

Bortezomib effectively suppresses drug resistance in K562/DNR cells by reducing NF-κB and P-gp expression. This proteasome inhibitor treatment also promotes cancer cell apoptosis in a dose- and time-dependent manner.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Pharmacology

Background:

  • Daunorubicin (DNR) induces drug resistance in K562 cells, associated with increased NF-κB and P-gp expression.
  • Understanding mechanisms of drug resistance is crucial for developing effective cancer therapies.

Purpose of the Study:

  • To investigate the effects of bortezomib (PS341) on NF-κB, IκB, and P-gp expression in daunorubicin-induced resistant K562 cells (K562/DNR).
  • To evaluate bortezomib's impact on K562/DNR cell apoptosis and drug resistance.

Main Methods:

  • MTT assay for drug resistance and bortezomib cytotoxicity.
  • Western blot to detect NF-κB, IκB, and P-gp expression.
  • Flow cytometry for apoptosis rate analysis.
  • ELISA for NF-κB activity detection.

Main Results:

  • DNR treatment significantly induced NF-κB and P-gp expression in K562/DNR cells.
  • Bortezomib treatment suppressed DNR-induced NF-κB and P-gp expression.
  • The suppressive effect of bortezomib was concentration- and time-dependent.

Conclusions:

  • Bortezomib, a proteasome inhibitor, can overcome cellular drug resistance.
  • Bortezomib promotes apoptosis in resistant cancer cells.
  • The observed effects of bortezomib are concentration- and time-dependent.

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