microRNA‑125b promotes leukemia cell resistance to daunorubicin by inhibiting apoptosis

Mol Med Rep. 2014 May;9(5):1909-16. doi: 10.3892/mmr.2014.2011. Epub 2014 Mar 6.

Abstract

microRNA-125b (miR-125b) is overexpressed in several types of cancer and contributes to tumor resistance to chemotherapy. The present study investigated the effect of miR-125b on the resistance of leukemia cell lines to the chemotherapeutic agent daunorubicin (DNR). miR-125b expression was found to be upregulated in patients who had failed therapy compared with those who demonstrated event-free survival. The overexpression of miR-125b was observed to induce DNR resistance in K562, THP‑1 and Jurkat cells by reducing apoptosis, whereas the suppression of miR-125b was found to enhance DNR cytotoxicity in REH cells. Furthermore, miR-125b was observed to mediate DNR resistance in leukemia cell lines through decreasing expression of G protein-coupled receptor kinase 2 and p53-upregulated modulator of apoptosis, which were shown to be direct targets of miR-125b using a dual-luciferase reporter. The present study provides a novel mechanism for understanding leukemia drug resistance and provides a novel method for calculating patient prognosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Apoptosis / drug effects*
  • Apoptosis / genetics*
  • Apoptosis Regulatory Proteins / genetics
  • Cell Line, Tumor
  • Daunorubicin / pharmacology*
  • Drug Resistance, Neoplasm / genetics*
  • Female
  • G-Protein-Coupled Receptor Kinase 2 / genetics
  • Gene Expression
  • Gene Expression Regulation, Leukemic
  • Gene Knockdown Techniques
  • Humans
  • Leukemia / diagnosis
  • Leukemia / genetics*
  • Male
  • MicroRNAs / genetics*
  • Middle Aged
  • Proto-Oncogene Proteins / genetics
  • Young Adult

Substances

  • Apoptosis Regulatory Proteins
  • BBC3 protein, human
  • MIRN125 microRNA, human
  • MicroRNAs
  • Proto-Oncogene Proteins
  • G-Protein-Coupled Receptor Kinase 2
  • Daunorubicin