Hypermethylation of the interferon regulatory factor 5 promoter in Epstein-Barr virus-associated gastric carcinoma

Seung Myung Dong; Hyun Gyu Lee; Sung-Gyu Cho; Seung-Hyun Kwon; Heejei Yoon; Hyun-Jin Kwon; Ji Hae Lee; Hyemi Kim; Pil-Gu Park; Hoguen Kim; S. Diane Hayward; Jeon Han Park; Jae Myun Lee

doi:10.1007/s12275-014-4654-3

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Hypermethylation of the interferon regulatory factor 5 promoter in Epstein-Barr virus-associated gastric carcinoma: Seung Myung Dong ¹, Hyun Gyu Lee ², Sung-Gyu Cho ², Seung-Hyun Kwon ², Heejei Yoon ², Hyun-Jin Kwon ², Ji Hae Lee ¹, Hyemi Kim ^2,3, Pil-Gu Park ², Hoguen Kim ^3,4, S. Diane Hayward ⁵, Jeon Han Park ², Jae Myun Lee ^2,3; Journal of Microbiology 2015;53(1):70-76.
DOI: https://doi.org/10.1007/s12275-014-4654-3
Published online: January 4, 2015

¹Research Institute, National Cancer Center, Goyang, Gyeonggi-do 410-769, Republic of Korea, ²Department of Microbiology and Immunology, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea, ³Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea, ⁴Department of Pathology, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea, ⁵Department of Oncology Johns Hopkins University School of Medicine, Baltimore, MD, USA¹Research Institute, National Cancer Center, Goyang, Gyeonggi-do 410-769, Republic of Korea, ²Department of Microbiology and Immunology, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea, ³Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea, ⁴Department of Pathology, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea, ⁵Department of Oncology Johns Hopkins University School of Medicine, Baltimore, MD, USA

Corresponding author: Jae Myun Lee , Tel: +82-2-2228-1822,

Received: 12 November 2014 • Revised: 26 November 2014 • Accepted: 27 November 2014

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Abstract

Interferon regulatory factor-5 (IRF-5), a member of the mammalian IRF transcription factor family, is regulated by p53, type I interferon and virus infection. IRF-5 participates in virus-induced TLR-mediated innate immune responses and may play a role as a tumor suppressor. It was suppressed in various EBV-infected transformed cells, thus it is valuable to identify the suppression mechanism. We focused on a promoter CpG islands methylation, a kind of epigenetic regulation in EBV-associated Burkitt’s lymphomas (BLs) and gastric carcinomas. IRF-5 is not detected in most of EBV-infected BL cell lines due to hypermethylation of IRF-5 distal promoter (promoter-A), which was restored by a demethylating agent, 5-aza-2􍿁-deoxycytidine. Hypomethylation of CpG islands in promoter-A was observed only in EBV type III latent infected BL cell lines (LCL and Mutu III). Similarly, during EBV infection to Akata-4E3 cells, IRF-5 was observed at early time periods (2 days to 8 weeks), concomitant unmethylation of promoter-A, but suppressed in later infection periods as observed in latency I BL cell lines. Moreover, hypermethylation in IRF-5 promoter-A region was also observed in EBV-associated gastric carcinoma (EBVaGC) cell lines or primary gastric carcinoma tissues, which show type I latent infection. In summary, IRF-5 is suppressed by hypermethylation of its promoter-A in most of EBV-infected transformed cells, especially BLs and EBVaGC. EBV-induced carcinogenesis takes an advantage of proliferative effects of TLR signaling, while limiting IRF-5 mediated negative effects in the establishment of EBVaGCs.

Keywords: interferon regulatory factor 5;Epstein-Barr virus;gastric carcinoma;CpG island;promoter methylation

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Hypermethylation of the interferon regulatory factor 5 promoter in Epstein-Barr virus-associated gastric carcinoma

J. Microbiol. 2015;53(1):70-76. Published online January 4, 2015

DOI: https://doi.org/10.1007/s12275-014-4654-3

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