MDV Oncogene Meq was Involved in Chicken Marek’s Disease Lymphoma Transformation

As an excellent study model of herpesvirus-induced tumor, Marek’s disease (MD) is highly cell-associated and contagious disease caused by an alpha herpesvirus. It could result in neural lesions, immunosuppression and neoplasias. Meq is an important oncogene which is highly expressed in MD tumor tissues and T-lymphoblastoid cell lines including MSB1 cell line. To elucidate mechanism of Meq on MD transformation, we used siRNA to interfere with its expression whose interference efficiency was about 60% in MSB1 cells. When Meq was interrupted, cell cycle was unaffected. However, Meq knockdown could promote cell apoptosis by regulating gene expression related to apoptosis in apoptotic pathway and TGF- ß pathway. After Meq intervention, pro-apoptotic TNFSF10 was upregulated but anti-apoptotic BCL2L1 and BCL2 were downregulated in apoptotic pathway; moreover, SPP1 and CREBBP were downregulated in TGF- ß pathway. In addition, cell migration had a downward trend after Meq knockdown. MMP2 and MMP9 expression closely related to invasion were decreased while Meq was interrupted. Meq was previously reported to bind to the promoter of IL-2 to promote its expression. In our study, IL-2 expression was greatly downregulated when Meq was interfered. Above all, Meq as an oncogene played an important role in MD tumor transformation.