Methylation of tumour suppressor genes APAF-1 and DAPK-1 and in vitro effects of demethylating agents in bladder and kidney cancer

Br J Cancer. 2006 Dec 18;95(12):1701-7. doi: 10.1038/sj.bjc.6603482. Epub 2006 Nov 28.

Abstract

To examine the significance of the methylation level of the p53 target and tumour suppressor genes apoptotic protease activating factor-1 (APAF-1) and death-associated protein kinase-1 (DAPK-1) in 80 microdissected tumour samples from transitional cell carcinoma (TCC) of the bladder and 80 tumour samples from clear-cell renal cell carcinoma (RCC) as well as from non-tumourous bladder and kidney tissue. Growth-inhibitory effects of the demethylating agents 5-Aza-2'-deoxycytidine (5-Aza-CdR) and zebularine were investigated in TCC and RCC cell lines. The methylation frequency of APAF-1 (DAPK-1) was 100% (77%) in TCC and 100% (33%) in RCC. The methylation levels of APAF-1 could differentiate between the individual tumour stages in TCC as well as in RCC. The APAF-1 methylation levels in RCC were significantly higher in tumours larger than 4 cm and in high-grade tumours. The methylation frequencies in normal tissue for APAF-1 (DAPK-1) were 11% (8%) in bladder tissue and 9% (5%) in kidney tissue. The growth-inhibitory effect of the demethylating agents in TCC (RT4, T24) and RCC (A498, ClearCa-5) cell lines resulted in a 17-132% prolongation of the doubling time (DT). In RCC cell lines, zebularine was superior to 5-Aza-CdR in achieving a DT prolongation. Quantitative real time RT-PCR detected a re-expression of mRNA transcripts of APAF-1 or DAPK-1. In conclusion, demethylating agents effectively retard growth of TCC and RCC cell lines. Methylation level analysis of specific genes has the potential for further tumour characterisation in TCC and RCC.

MeSH terms

  • Aged
  • Antimetabolites, Antineoplastic / pharmacology
  • Apoptosis Regulatory Proteins / genetics*
  • Apoptosis Regulatory Proteins / metabolism
  • Apoptotic Protease-Activating Factor 1 / genetics*
  • Apoptotic Protease-Activating Factor 1 / metabolism
  • Azacitidine / chemistry
  • Azacitidine / pharmacology*
  • Calcium-Calmodulin-Dependent Protein Kinases / genetics*
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism
  • Carcinoma, Renal Cell / genetics
  • Carcinoma, Transitional Cell / genetics
  • Cells, Cultured
  • Cytidine / analogs & derivatives*
  • Cytidine / pharmacology
  • DNA Methylation*
  • Death-Associated Protein Kinases
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • In Vitro Techniques
  • Kidney / cytology
  • Kidney / drug effects
  • Kidney / metabolism
  • Kidney Neoplasms / genetics*
  • Male
  • Promoter Regions, Genetic / genetics
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Urinary Bladder / cytology
  • Urinary Bladder / drug effects
  • Urinary Bladder / metabolism
  • Urinary Bladder Neoplasms / genetics*

Substances

  • APAF1 protein, human
  • Antimetabolites, Antineoplastic
  • Apoptosis Regulatory Proteins
  • Apoptotic Protease-Activating Factor 1
  • RNA, Messenger
  • Cytidine
  • pyrimidin-2-one beta-ribofuranoside
  • DAPK1 protein, human
  • Death-Associated Protein Kinases
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Azacitidine