[Reversal effect of 5-Aza-dc on cisplatin-resistance in human NSCLC cells in vitro]

Zhonghua Zhong Liu Za Zhi. 2011 May;33(5):349-53.
[Article in Chinese]

Abstract

Objective: The aim of this study was to investigate the effect of 5-aza-2'-deoxycytidine (5-Aza-dc), a methylation inhibitor, on cisplatin-resistance in non-small cell lung cancer cell line A549/DDP and to explore its possible mechanism.

Methods: MTT assay was used to test the cytotoxicity of 5-Aza-dc on A549/DDP cells, and the IC(50) and cisplatin resistance index of A540/DDP cells at 48 hours after 5-Aza-dc (0 µmol/L, 20 µmol/L, 40 µmol/L) treatment at different concentrations. MSP, fluorescence quantitative RT-PCR (real-time RT-PCR) and Western blot were used to detect the hMLH1 methylation status, mRNA and protein expressions, respectively.

Results: The IC(50) value of cisplatin in A549/DDP cells was 30.15 ± 0.76 µmol/L. The MTT assay results demonstrated that during the 5-Aza-dc treatment for 48 hours, the dose of 20 µmol/L was non-toxic and 40 µmol/L was low-toxic. 5-Aza-dc at those two doses reduced IC(50) value of cisplatin to 16.54 ± 0.35 µmol/L (RI = 1.82) and 6.82 ± 0.16 µmol/L (RI = 4.42), respectively. MSP, real-time RT-PCR and Western blot showed that 5-Aza-dc at non-toxic and low-toxic doses removed the partial hMLH1-hypermethylation, and up-regulated hMLH1 mRNA and protein expressions.

Conclusions: Low dose 5-Aza-dc can partially reverse the cisplatin-resistance in A549/DDP cells, which may be achieved through removal of hMLH1 hypermethylation and increased expression of hMLH1 gene. 5-Aza-dc may have a role in increasing the efficacy of chemotherapy for patients whose tumors are lack of hMLH1 expression because of hMLH1 promoter hypermethylation.

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / metabolism*
  • Antimetabolites, Antineoplastic / administration & dosage
  • Antimetabolites, Antineoplastic / pharmacology*
  • Azacitidine / administration & dosage
  • Azacitidine / analogs & derivatives*
  • Azacitidine / pharmacology
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / pathology*
  • Cell Line, Tumor
  • Cisplatin / pharmacology
  • DNA Methylation
  • Decitabine
  • Dose-Response Relationship, Drug
  • Drug Resistance, Neoplasm
  • Humans
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology*
  • MutL Protein Homolog 1
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Promoter Regions, Genetic / genetics
  • RNA, Messenger / metabolism

Substances

  • Adaptor Proteins, Signal Transducing
  • Antimetabolites, Antineoplastic
  • MLH1 protein, human
  • Nuclear Proteins
  • RNA, Messenger
  • Decitabine
  • MutL Protein Homolog 1
  • Azacitidine
  • Cisplatin