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Methylation-associated silencing of SFRP1 in renal cell carcinoma

Yasuo Awakura1, Eijiro Nakamura, Noriyuki Ito

  • 1Department of Urology, Kyoto University Graduate School of Medicine, Kyoto, Japan.

Oncology Reports
|October 25, 2008
PubMed

Insights

Secreted frizzled-related protein 1 (SFRP1) silencing by promoter hypermethylation is frequent in renal cell carcinoma (RCC). This epigenetic inactivation of SFRP1, a tumor suppressor, likely plays a key role in kidney cancer development.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Secreted frizzled-related protein 1 (SFRP1) is a tumor suppressor gene that inhibits Wnt signaling.
  • Epigenetic silencing of SFRP1 via promoter methylation is implicated in various cancers.
  • The role of SFRP1 in renal cell carcinoma (RCC) remains to be fully elucidated.

Purpose of the Study:

  • To investigate the expression and methylation status of SFRP1 in RCC.
  • To determine the association between SFRP1 promoter methylation and its expression in RCC.
  • To assess the frequency of SFRP1 alterations in RCC development.

Main Methods:

  • Analysis of SFRP1 transcript expression in RCC cell lines.
  • Bisulfite sequencing and methylation-specific PCR for SFRP1 promoter methylation analysis.
  • Quantitative real-time PCR for SFRP1 expression levels.
  • Microsatellite analysis for loss of heterozygosity at the SFRP1 locus.

Main Results:

  • SFRP1 expression was undetectable in tested RCC cell lines.
  • SFRP1 promoter hypermethylation was detected in 45.6% of conventional RCC and 25% of papillary RCC cases.
  • A significant decrease in SFRP1 expression (>3-fold) was observed in 97.1% of conventional RCC cases.
  • Loss of heterozygosity at the SFRP1 locus was infrequent (10.7% in conventional RCC).

Conclusions:

  • Methylation-associated silencing of SFRP1 is a common event in RCC.
  • SFRP1 inactivation likely contributes to kidney cancer initiation.
  • Further research is needed to understand SFRP1's role in Wnt and other signaling pathways in RCC, especially given conflicting data on beta-catenin activation.

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