Abstract
Correlation of Epstein-Barr virus copy numbers, MICA expression and rs2596542 variant in nasopharyngeal carcinoma tumour
Thanh Dat Ta1, Khanh Tran Van1, 2, Thanh Binh Nguyen3, Manh Thuong Le4, Long Ha Le Hai2, Hoang Viet Nguyen1, 2*
1Center for Gene-Protein Research, Hanoi Medical University
2Faculty of Medical Technology, Hanoi Medical University
3Department of Pathophysiology and Immunology, Hanoi Medical University
4Department of Anatomy, Hanoi Medical University
Received 4 March 2022; accepted 25 April 2022
Abstract:
Major histocompatibility complex class I chain-related A (MICA) is a tumour antigen that is greatly expressed on the surfaces of human malignancies and infection cells, which trigger attachment to immune cells. Although many studies have investigated the role of the MICA rs2596542 variant involved in high risk of hepatocellular carcinoma (HCC), the expression regulation of rs2596542 MICA in nasopharyngeal carcinoma (NPC) susceptibility with the Epstein-Barr virus (EBV) is still ambiguous. Therefore, this study was conducted to elucidate the association of rs2596542C/T and EBV load to MICA expression in NPC tissues. A total of 70 tumour tissues from NPC patients were enrolled in the current study. The genetic variant of rs2596542 was identified by Real-time PCR genotyping, and MICA protein expression was quantified by immunohistochemistry staining. A significant difference was observed in the expression of MICA regarding EBV copy numbers (p<0.01). High expression of MICA presented a considerably lower EBV status. In addition, higher expression of homologous MICA rs2596542 CC was significantly associated with a lower EBV load (p<0.001) thus suggesting a protective role of allele C against the infection of EBV. In summary, rs2596542 MICA plays an important role in the immune response preventing the EBV among NPC patients as well as developing a new predictive biomarker for virus susceptibility to cancers.
Keywords: Epstein-Barr virus (EBV), MICA expression, rs2596542.
Classification number: 3.2



