Knockdown of nucleophosmin by RNA interference reverses multidrug resistance in resistant leukemic HL-60 cells

Immunobiology. 2013 Sep;218(9):1147-54. doi: 10.1016/j.imbio.2013.04.001. Epub 2013 Apr 10.

Abstract

Nucleophosmin, a multifunctional nucleolar phosphoprotein, is involved in many cellular activities. However, the role of NPM in drug-resistance of leukemia has not yet been explored. We designed and selected one shRNA targeting on NPM gene transduction into HL-60 and HL-60/ADR cell lines (an adriamycin resistant cell line) by lentivirus. Cell proliferation, apoptosis and differentiation were assessed. The expressions of the related genes and proteins were detected by real-time quantitative RT-PCR and Western blotting. The results showed obvious down-regulation of NPM mRNA and protein levels after NPM RNAi. NPM-targeted RNAi also resulted in many cellular changes, such as, suppressing cell proliferation and inducing cell differentiation. Down-regulation of NPM gene could arrest the cell cycle progression, an increase in the proportion of G0/G1 phase in knockdown groups. NPM gene silencing could also induce pro-apoptotic genes and proteins expression, and inhibit anti-apoptotic genes/proteins expression. Furthermore, IC50 of two chemotherapeutic agents (adriamycin and ADR; daunorubicin and DNR) to HL-60 and HL-60/ADR cells decreased, especially more remarkable on HL-60/ADR cells. IC50 of ADR on HL-60/ADR cells was reduced from 12.544 ± 0.851 μmol/L (before NPM RNAi) to 6.331 ± 0.522 μmol/L (after NPM RNAi), IC50 of DNR was reduced from 2.152 ± 0.143 μmol/L (before NPM RNAi) to 1.116 ± 0.093 μmol/L (after NPM RNAi). The relative reversal rate of HL-60/ADR cells on ADR was 50.2%, and on DNR was 48.9%. In conclusion, our results demonstrated that shRNA expression vectors could effectively reduce NPM expression and restore the drug sensitivity of resistant leukemic cells to conventional chemotherapeutic agents.

Keywords: 12-O-tetradecanoylphorbol-13-acetate; ADR; AML; DNR; ECL; IC50; LV; Leukemia; MDR; Multidrug resistance; NBT; NPM; Nucleophosmin; PI; RNA interference; RNAi; RR; TPA; VCR; VP16; acute myeloid leukemia; adriamycin; daunorubicin; enhanced chemiluminescence; etoposide; half inhibitory concentration; lentivirus; multidrug resistance; nitroblue tetrazolium reduction; nucleophosmin; propidium iodide; qRT-PCR; quantitative real-time reverse transcription chain reaction; relative reversal rate; shRNA; short hairpin RNA; vincristine.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / therapeutic use
  • Apoptosis / genetics
  • Cell Differentiation / genetics
  • Cell Growth Processes / genetics
  • Doxorubicin / therapeutic use
  • Drug Resistance, Multiple / genetics*
  • Drug Resistance, Neoplasm / genetics*
  • Gene Knockdown Techniques
  • Genetic Vectors / genetics
  • HL-60 Cells
  • Humans
  • Lentivirus
  • Leukemia, Promyelocytic, Acute / drug therapy*
  • Leukemia, Promyelocytic, Acute / pathology
  • Nuclear Proteins / genetics*
  • Nucleophosmin
  • RNA Interference
  • RNA, Small Interfering / genetics

Substances

  • Antineoplastic Agents
  • NPM1 protein, human
  • Nuclear Proteins
  • RNA, Small Interfering
  • Nucleophosmin
  • Doxorubicin