## 1 Introduction  
Gastric carcinoma is a significant global health concern, with various etiological factors contributing to its development. Among these, Epstein-Barr virus (EBV) infection has been identified as a key factor in a subset of gastric cancers, referred to as EBV-associated gastric carcinoma (EBVAGC) [1]. EBVaGC exhibits distinct molecular and clinical features, including unique immune evasion mechanisms and altered signaling pathways. Epstein-Barr virus is a ubiquitous herpesvirus that infects over 90% of the world's population and establishes a lifelong latent infection within the host [2]. EBV is primarily transmitted through saliva and typically infects B lymphocytes and epithelial cells. Infected cells can harbor the virus in a latent state, during which the viral genome persists as an episome within the nucleus of the host cell, expressing a limited set of viral proteins that contribute to oncogenesis and immune evasion [3]. The latency-associated proteins, including EBV nuclear antigen 1 (EBNA1), latent membrane proteins (LMPs), and Epstein-Barr-encoded small RNAs (EBERs), are crucial for maintaining viral persistence and promoting cell proliferation [4]. A notable feature of EBVaGC is the expression of _EBNA1_, which is critical for the maintenance of the viral genome within infected cells. EBNA1 is known for its strong antigenicity, which can elicit immune responses, although the virus employs various strategies to evade immune detection [5]. Androgens, including dihydrotestosterone (DHT), play crucial roles in various physiological processes and have been implicated in the regulation of immune responses [6]. Androgen signaling occurs through the androgen receptor (AR), a type of nuclear receptor that, upon binding to androgens, translocates to the nucleus and influences gene expression [7]. The AR-DHT signaling pathway is pivotal in numerous biological processes, including the development and maintenance of male characteristics, the regulation of libido, and the modulation of muscle mass and bone density [8]. Additionally, AR-DHT signaling has been shown to influence cell proliferation, differentiation, and apoptosis, thereby playing a significant role in various cancers, including prostate [9] and gastric cancers. Recent studies have suggested that DHT can modulate immune function by influencing signaling pathways within target cells, including the NF-\(\kappa\)B pathway [10; 11]. NF-\(\kappa\)B is a key regulator of immune and inflammatory responses, controlling the expression of various genes involved in immune responses, cell proliferation, and survival [10]. This makes NF-\(\kappa\)B a critical player in cancer progression and immune system interactions. In this study, we investigate the effect of DHT on the expression of MHC class I-related chain A (_MICA_) in SNU719 cells, a human gastric cancer cell line derived from EBV-associated gastric carcinoma. MICA is a stress-induced ligand that is recognized by the NKG2D receptor on natural killer (NK) and CD8+ T cells [12]. NKG2D is an activating receptor that plays a crucial role in the immune system's ability to detect and eliminate stressed, transformed, or infected cells [13]. The interaction between MICA and NKG2D triggers the cytotoxic activity of these immune cells, enhancing their ability to target and destroy tumor cells. Our findings demonstrate that treatment with DHT leads to the upregulation of NF-\(\kappa\)B, mediated by androgen receptor signaling, which in turn increases the expression of _MICA_ in SNU719 cells. This increase in MICA expression enhances the ability of NK and CD8+ T cells to identify and attack SNU719 cells, making the tumor cells more vulnerable to immune-mediated cytotoxicity. Understanding the mechanisms by which DHT influences _MICA_ expression and the subsequent immune response in the context of EBVaGC can provide valuable insights into potential therapeutic strategies for enhancing anti-tumor immunity.