Aspirin enhances multidrug resistance gene 1 expression in human Molt-4 T lymphoma cells

Anticancer Res. 2000 Nov-Dec;20(6B):4441-4.

Abstract

Background: We recently found that aspirin induces the expression of P-glycoprotein (P-gp), a protein mediating drug resistance, in human prostate cancer cells. The purpose of this study was to evaluate the effect of aspirin on the expression of P-gp in a different human cancer type, i.e., T lymphoma. Furthermore, we analyzed this effect at the level of the gene encoding P-gp, MDR1, and of the transcription factor (NF-IL6), regulating this gene.

Materials and methods: NF-IL6 was assayed by the electrophoretic mobility shift assay, MDR1 mRNA was assayed by the reverse transcriptase polymerase chain reaction (RT-PCR), and P-gp was assayed by Western blotting.

Results: aspirin, at plasma attainable levels, induced NF-IL6 DNA-binding activity, and increased MDR1 mRNA expression (by up to 140%), as well as the expression of P-gp, in Molt-4 cells.

Conclusions: This study suggests that treatment with aspirin induces a cellular signal culminating in the enhancement of P-gp expression in T lymphoma Molt-4 cells.

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B, Member 1 / genetics
  • ATP Binding Cassette Transporter, Subfamily B, Member 1 / metabolism*
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Aspirin / pharmacology*
  • CCAAT-Enhancer-Binding Protein-beta / metabolism
  • DNA, Neoplasm / metabolism
  • Gene Expression / drug effects*
  • Genes, MDR / drug effects*
  • Humans
  • Lymphoma, T-Cell / genetics
  • Lymphoma, T-Cell / metabolism*
  • RNA, Messenger / metabolism
  • Tumor Cells, Cultured / drug effects

Substances

  • ATP Binding Cassette Transporter, Subfamily B, Member 1
  • Anti-Inflammatory Agents, Non-Steroidal
  • CCAAT-Enhancer-Binding Protein-beta
  • DNA, Neoplasm
  • RNA, Messenger
  • Aspirin