Shekari Najibeh, Shanehbandi Dariush, Baghbani Elham, Safaei Sahar, Masoumi Javad, Baradaran Behzad, Jalali Seyed Amir
Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Naunyn Schmiedebergs Arch Pharmacol. 2025 Apr;398(4):3861-3880. doi: 10.1007/s00210-024-03491-z. Epub 2024 Oct 4.
VISTA is a newly discovered immune checkpoint whose functional mechanisms have become increasingly important to study due to its brilliant results in cancer immunotherapy. Despite VSIG-3/IGSF11 being identified as an inhibitory ligand for VISTA with potential as a target for cancer immunotherapy, very little is known of its functions. This study aimed to conduct a detailed analysis of VSIG-3/IGSF11 in melanoma, as well as to study the effects of its silencing on melanoma cell line progression and human T cell functions. Online databases were used to investigate VSIG-3/IGSF11 expression, its relationships, and prognostic value in melanoma. Then, the effects of VSIG-3/IGSF11 silencing on proliferation, migration, cell cycle arrest, and apoptosis in A2058 melanoma cells were assessed using MTT, colony formation, wound healing, cell cycle, and Annexin-V FITC/PI assays, respectively. Finally, A2058 cells transfected with VSIG-3/IGSF11 siRNA were co-cultured with human T cells, and the expression levels of T cell cytokines were evaluated using qRT-PCR. VSIG-3/IGSF11 expression was significantly increased in melanoma patients and cell lines; however, no correlation was found between VSIG-3/IGSF11 expression levels and clinicopathological characteristics, survival, or immune cell infiltration. Following VSIG-3/IGSF11 silencing in A2058 cells, viability, proliferation, and migration rates were decreased, while apoptosis was increased. T cells co-cultured with VSIG-3/IGSF11 siRNA-transfected A2058 cells exhibited increased expression levels of IFN-γ and IL-12 and decreased expression levels of IL-10, TGF-β, and TNF-α. The inhibitory effect of VSIG-3/IGSF11 silencing on A2058 melanoma cell progression, along with the alteration of T cell cytokines towards a pro-inflammatory phenotype, suggests that VSIG-3/IGSF11 is primarily involved in melanoma progression and modulating immune responses. Therefore, it may be a valuable target for immunotherapy in melanoma patients.
VISTA是一种新发现的免疫检查点,由于其在癌症免疫治疗中取得的出色成果,其功能机制的研究变得越来越重要。尽管VSIG-3/IGSF11被确定为VISTA的抑制性配体,具有作为癌症免疫治疗靶点的潜力,但其功能却鲜为人知。本研究旨在对黑色素瘤中的VSIG-3/IGSF11进行详细分析,并研究其沉默对黑色素瘤细胞系进展和人T细胞功能的影响。利用在线数据库研究VSIG-3/IGSF11在黑色素瘤中的表达、其相关性及预后价值。然后,分别使用MTT法、集落形成法、伤口愈合法、细胞周期法和膜联蛋白-V FITC/PI法评估VSIG-3/IGSF11沉默对A2058黑色素瘤细胞增殖、迁移、细胞周期阻滞和凋亡的影响。最后,将转染了VSIG-3/IGSF11 siRNA的A2058细胞与人T细胞共培养,并使用qRT-PCR评估T细胞细胞因子的表达水平。VSIG-3/IGSF11在黑色素瘤患者和细胞系中的表达显著增加;然而,未发现VSIG-3/IGSF11表达水平与临床病理特征、生存率或免疫细胞浸润之间存在相关性。在A2058细胞中沉默VSIG-3/IGSF11后,细胞活力、增殖和迁移率降低,而凋亡增加。与转染了VSIG-3/IGSF11 siRNA的A2058细胞共培养的T细胞表现出IFN-γ和IL-12表达水平升高,以及IL-10、TGF-β和TNF-α表达水平降低。VSIG-3/IGSF11沉默对A2058黑色素瘤细胞进展的抑制作用,以及T细胞细胞因子向促炎表型的改变,表明VSIG-3/IGSF11主要参与黑色素瘤进展并调节免疫反应。因此,它可能是黑色素瘤患者免疫治疗的一个有价值的靶点。