Epigenetic silencing of TNFSF7 (CD70) by DNA methylation during progression to breast cancer

Seung Eun Yu, Su Hyung Park, Yeun Kyu Jang

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

To escape the immune system, tumor cells may remove surface molecules such as the major histocompatibility complex (MHC) and co-stimulatory molecules, which are essential for recognition by lymphocytes. Down-regulation of the co-stimulatory molecules CD70 (TNFSF7) and CD80 may contribute to tumor cell survival; however, the mechanism of down-regulation of the TNFSF7 gene during tumorigenesis is poorly understood. Here we present evidence indicating that TNFSF7 gene expression is epigenetically down-regulated via DNA hypermethylation within its promoter region during progression in breast cancer cells in the isogenic MCF10 model. Bisulfite sequencing revealed that the CpG pairs at the proximal region of the TNFSF7 promoter are heavily methylated during progression of breast cancer cells but that methylation of the more distal sequences was not changed considerably. Thus, this epigenetic silencing of the TNFSF7 gene via hypermethylation of its proximal region may allow the benign and invasive MCF10 variants to escape immune surveillance.

Original languageEnglish
Pages (from-to)217-221
Number of pages5
JournalMolecules and cells
Volume29
Issue number2
DOIs
Publication statusPublished - 2010 Feb 1

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DNA Methylation
Epigenomics
Breast Neoplasms
Genetic Promoter Regions
Down-Regulation
Tumor Escape
Gene Silencing
Major Histocompatibility Complex
Methylation
Immune System
Cell Survival
Carcinogenesis
Lymphocytes
Gene Expression
DNA
Genes
Neoplasms

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

Cite this

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Epigenetic silencing of TNFSF7 (CD70) by DNA methylation during progression to breast cancer. / Yu, Seung Eun; Park, Su Hyung; Jang, Yeun Kyu.

In: Molecules and cells, Vol. 29, No. 2, 01.02.2010, p. 217-221.

Research output: Contribution to journalArticle

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