Hypomethylation upregulates the expression of CD30 in lymphoma induced by Marek's disease virus

Epigenetic modification is widely known to be involved in embryo development, aging, tumorigenesis, and many complex diseases. Both hypermethylation of CpG islands at the gene promoters and global hypomethylation are involved in the initiation and progression of carcinogenesis. However, only a small portion of hypomethylation occurs at gene promoters and leads to the overexpression of certain oncogenes. To determine whether DNA methylation plays a role in tumorigenesis of Marek's disease, we selected one putative oncogene and 8 tumor suppressor genes from the gene expression profile for the analysis of DNA methylation variation. Four normal spleen tissues and 4 Marek's disease virus-infected tumor spleen tissues were collected, and the methylation level of the promoter region of each gene was analyzed using MassARRAY. As a result, the promoter region of CD30 was hypomethylated and displayed a significantly higher expression in Marek's disease virus-infected tumor spleen tissues compared with normal ones (P < 0.05). In neoplastic cells, CD30 was known to promote the survival and proliferation of T-cell lymphomas. This result suggests that activation of CD30 is possibly associated with the tumorigenesis of Marek's disease.