Abstract
Epstein-Barr virus (EBV) is responsible for the development of multiple tumors, including EBV-associated gastric carcinoma (EBVaGC), but little is known about its mechanisms in EBVaGC. WNT5A expression and promoter methylation were measured in 5 EBV-positive and 15 EBV-negative GC cell lines. The methylation status of 23 EBV-positive and 25 EBV-negative paired tumor/normal tissue samples was also examined. EBV-positive GC had no or very low expression of WNT5A but a high level of methylation in the promoter region. In contrast, EBV-negative GC had higher WNT5A expression and a lower level of promoter methylation. The reduced WNT5A expression could be restored by treatment with Aza, a methyltransferase inhibitor. Increased expression of WNT5Ain vitro inhibited β-catentin expression in EBVaGC cells (SNU719). These results suggest that hypermethylation of WNT5A induced by EBV may contribute to the development of EBVaGC. Ectopic introduction of WNT5A may have preventive/therapeutic potential for tumors with silenced WNT5A.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 123-132 |
| Number of pages | 10 |
| Journal | Archives of Virology |
| Volume | 158 |
| Issue number | 1 |
| DOIs | |
| State | Published - 2013 |
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ASJC Scopus subject areas
- Virology
Cite this
Epigenetic silencing of WNT5A in Epstein-Barr virus-associated gastric carcinoma. / Liu, Xia; Wang, Yun; Wang, Xiaofeng; Sun, Zhifu D; Li, Lili; Tao, Qian; Luo, Bing.
In: Archives of Virology, Vol. 158, No. 1, 2013, p. 123-132.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Epigenetic silencing of WNT5A in Epstein-Barr virus-associated gastric carcinoma
AU - Liu, Xia
AU - Wang, Yun
AU - Wang, Xiaofeng
AU - Sun, Zhifu D
AU - Li, Lili
AU - Tao, Qian
AU - Luo, Bing
PY - 2013
Y1 - 2013
N2 - Epstein-Barr virus (EBV) is responsible for the development of multiple tumors, including EBV-associated gastric carcinoma (EBVaGC), but little is known about its mechanisms in EBVaGC. WNT5A expression and promoter methylation were measured in 5 EBV-positive and 15 EBV-negative GC cell lines. The methylation status of 23 EBV-positive and 25 EBV-negative paired tumor/normal tissue samples was also examined. EBV-positive GC had no or very low expression of WNT5A but a high level of methylation in the promoter region. In contrast, EBV-negative GC had higher WNT5A expression and a lower level of promoter methylation. The reduced WNT5A expression could be restored by treatment with Aza, a methyltransferase inhibitor. Increased expression of WNT5Ain vitro inhibited β-catentin expression in EBVaGC cells (SNU719). These results suggest that hypermethylation of WNT5A induced by EBV may contribute to the development of EBVaGC. Ectopic introduction of WNT5A may have preventive/therapeutic potential for tumors with silenced WNT5A.
AB - Epstein-Barr virus (EBV) is responsible for the development of multiple tumors, including EBV-associated gastric carcinoma (EBVaGC), but little is known about its mechanisms in EBVaGC. WNT5A expression and promoter methylation were measured in 5 EBV-positive and 15 EBV-negative GC cell lines. The methylation status of 23 EBV-positive and 25 EBV-negative paired tumor/normal tissue samples was also examined. EBV-positive GC had no or very low expression of WNT5A but a high level of methylation in the promoter region. In contrast, EBV-negative GC had higher WNT5A expression and a lower level of promoter methylation. The reduced WNT5A expression could be restored by treatment with Aza, a methyltransferase inhibitor. Increased expression of WNT5Ain vitro inhibited β-catentin expression in EBVaGC cells (SNU719). These results suggest that hypermethylation of WNT5A induced by EBV may contribute to the development of EBVaGC. Ectopic introduction of WNT5A may have preventive/therapeutic potential for tumors with silenced WNT5A.
UR - http://www.scopus.com/inward/record.url?scp=84872263647&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84872263647&partnerID=8YFLogxK
U2 - 10.1007/s00705-012-1481-x
DO - 10.1007/s00705-012-1481-x
M3 - Article
C2 - 23001722
AN - SCOPUS:84872263647
VL - 158
SP - 123
EP - 132
JO - Archives of Virology
JF - Archives of Virology
SN - 0304-8608
IS - 1
ER -