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 language | English |
|---|---|
| Pages (from-to) | 217-221 |
| Number of pages | 5 |
| Journal | Molecules and cells |
| Volume | 29 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2010 Feb 1 |
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All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology
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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 journal › Article
TY - JOUR
T1 - Epigenetic silencing of TNFSF7 (CD70) by DNA methylation during progression to breast cancer
AU - Yu, Seung Eun
AU - Park, Su Hyung
AU - Jang, Yeun Kyu
PY - 2010/2/1
Y1 - 2010/2/1
N2 - 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.
AB - 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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U2 - 10.1007/s10059-010-0052-9
DO - 10.1007/s10059-010-0052-9
M3 - Article
VL - 29
SP - 217
EP - 221
JO - Molecules and Cells
JF - Molecules and Cells
SN - 1016-8478
IS - 2
ER -