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

Molecules and Cells
Seung Eun YuYeun Kyu Jang

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.

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Citations

Jan 13, 2015·Expert Review of Clinical Immunology·Xiang LiWeidong Han
Sep 25, 2012·Biochemical and Biophysical Research Communications·Seung Eun Yu, Yeun Kyu Jang
Mar 6, 2012·Clinical Immunology : the Official Journal of the Clinical Immunology Society·Christian M Hedrich, Thomas Rauen
Jul 28, 2015·Pharmacology & Therapeutics·J JacobsP Pauwels
Jan 24, 2017·Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology·Leandro Cerchietti, Ari Melnick
Nov 26, 2013·The Cancer Journal·Tomasz MajWeiping Zou
Aug 10, 2017·Journal of Neuropathology and Experimental Neurology·Drew PrattMartha Quezado
Feb 19, 2015·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Melanie RufPeter Schraml

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