UNDERSTANDING THE ROLE OF NZF3 IN THE IMMUNOSUPPRESSIVE EFFECTS OF ANISOMYCIN ON T CELLS
Keywords:
Anisomycin, Chemotherapy, Inflammatory Responses, NZF3, siRNA, T cellsAbstract
Anisomycin, a protein synthesis inhibitor with potential chemotherapeutic applications, has been shown to inhibit inflammatory responses and the activation of T cells, reducing its potential anti-cancer effect. NZF3, a transcription factor, on the other hand, enhances inflammation and the expression of proinflammatory genes. This study aimed to investigate the impact of knocking down the NZF3 gene in T cells on the immunosuppressive effects of anisomycin. The study employed a method for knocking down NZF3 using siRNA in T cells. Results indicated that the knockdown of the NZF3 gene partially reversed the immunosuppressive effects induced by anisomycin. Specifically, colony formation, CD69, CD25, and CD71 expression, and secretion of pro-inflammatory cytokines were increased. These findings suggest that NZF3 may be a potential target to optimize the use of anisomycin for cancer treatment and provide new insight into combination therapies utilizing anisomycin