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Estrogen receptor-binding fragment-associated gene 9 (EBAG9), also known as Receptor-binding cancer antigen expressed on SiSo cells (RCAS1), is a type II transmembrane protein that plays a pivotal role in tumor immune evasion [1, 3]. The EBAG9 mRNA transcript is an estrogen-responsive target primarily expressed in the Golgi apparatus, where the resulting protein participates in vesicle trafficking and protein secretion [1, 2]. In many human cancers, EBAG9 is significantly overexpressed, leading to the induction of apoptosis in surrounding immune cells, such as T-lymphocytes and natural killer (NK) cells [3, 4]. Targeting EBAG9 mRNA using siRNA or antisense oligonucleotides is an experimental therapeutic approach designed to silence the gene and restore the activity of the immune system against malignant cells [5]. By degrading the EBAG9 mRNA or blocking its translation, these therapies aim to reduce the immunosuppressive environment created by the tumor [4, 5]. Clinical interest in EBAG9 also stems from its potential as a prognostic biomarker, as high mRNA and protein levels often correlate with advanced disease stages and poor patient outcomes [4]. Research continues to evaluate how silencing EBAG9 mRNA can enhance the efficacy of other immunotherapies [5].
Inhibition of EBAG9 mRNA translation or promotion of its degradation to reduce EBAG9 protein levels, thereby preventing tumor-induced apoptosis of immune cells and enhancing anti-tumor immunity.
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