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Two CpG islands in the SEMA3B gene: Methylation in clear cell renal cell carcinoma

Authors
  • Loginov, V. I.1
  • Khodyrev, D. S.1
  • Pronina, I. V.1, 2
  • Malyukova, A. V.1, 3
  • Kazubskaya, T. P.4
  • Ermilova, V. D.4
  • Gar’kavtseva, R. F.4
  • Zabarovskii, E. R.2, 3
  • Braga, E. A.1
  • 1 State Research Center GosNIIgenetika, Moscow, 117545, Russia , Moscow (Russia)
  • 2 Russian Academy of Sciences, Engelgardt Institute of Molecular Biology, Moscow, 119991, Russia , Moscow (Russia)
  • 3 Karolinska Institute, Microbiology, Cell Biology and Tumor Biology Center, Stockholm, 17177, Sweden , Stockholm (Sweden)
  • 4 Russian Academy of Medical Sciences, N.N. Blokhin Russian Cancer Research Center, Moscow, 115478, Russia , Moscow (Russia)
Type
Published Article
Journal
Molecular Biology
Publisher
Pleiades Publishing
Publication Date
Dec 04, 2009
Volume
43
Issue
6
Identifiers
DOI: 10.1134/S0026893309060156
Source
Springer Nature
Keywords
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Abstract

Earlier, methylation of a CpG island in the SEMA3B gene (3p21.31) was observed in cell lines of small-cell and non-small-cell lung carcinoma. According to NCBI (Build 36), that island belonged to intron 1 of the gene. Our study concerns the methylation of two CpG islands, promoter and intronic, in the SEMA3B gene in patients with clear cell renal cell carcinoma (RCC). Methylation-specific PCR and bisulfite sequencing revealed a high frequency of methylation in the promoter CpG island (34/61, 56%) and somewhat lower, in the intronic (17/48, 35%). A significant inverse correlation was found between the SEMA3B mRNA level and methylation of the promoter CpG island in RCC (P < 0.05 according to Fisher’s exact test). The intronic island showed no such correlation. Thus, we suggest that the methylation of the promoter CpG island contributes to the inactivation of the SEMA3B suppressor gene in RCC tissue.

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