垂体瘤是源自垂体腺激素产生细胞的良性新生物。虽然大多数亚型已出现医疗治疗方案，但表达卵泡刺激素（FSH）和/或黄体生成素的促性腺细胞瘤外，仍缺乏治疗选择。激活素配体是促性腺细胞的FSH生成和分泌的生理调节因子，但它们在兴奋素致瘤的作用仍鲜为人知。采用产生FSH的LβT2小鼠促性腺细胞系，在兴奋素刺激下皮下移植到Rag2KO小鼠中，首先测试了LβT2细胞的皮下移植是否会导致肿瘤形成。组织学分析确认了存在于其微环境中的内皮细胞和巨噬细胞的LβT2肿瘤。FSH在瘤体中的LβT2细胞的一部分聚集中发现其表达。随后，我们通过注射可溶性激活素拦截受体（sActRIIB-Fc）来研究靶向兴奋素信号的后果。sActRIIB-Fc处理导致显著降低的LβT2肿瘤体积。减少的Smad2磷酸化以及对肿瘤诱导的FSH产生的抑制确认了该处理方式对兴奋素下游信号的有效靶向。更有趣的是，经过处理的肿瘤与减少的Vegfa表达相关的内皮细胞显著减少。LβT2细胞的sActRIIB-Fc体外处理对细胞增殖或凋亡没有影响，但抑制了Vegfa的表达，表明LβT2细胞通过兴奋素介导的Vegfa调节可能存在着可能的旁分泌效应作用于内皮细胞。需要进一步的体外和体内研究来确定兴奋素信号在这些过程中的确切作用，然后才能将这些观察结果转化为临床。

Pituitary tumours are benign neoplasms that derive from hormone-producing cells of the pituitary gland. While medical treatments have emerged for most subtypes, gonadotroph tumours that express follicle-stimulating hormone (FSH) and/or luteinizing hormone still lack therapeutic options apart from surgery and radiotherapy. Activin ligands are physiological regulators of production and secretion of FSH by gonadotroph cells, but their role in gonadotroph tumourigenesis remains little explored. Using the LβT2 mouse gonadotroph cell line which produces FSH under activin stimulation, we first tested whether subcutaneous xenografts of LβT2 cells resulted in tumour formation in Rag2KO mice. Histological analysis confirmed the presence of LβT2 tumours with endothelial cells and macrophages in their microenvironment. FSH expression was found in a subset of clusters of LβT2 cells in the tumours. We subsequently addressed the consequences of targeting activin signalling via injection of a soluble activin decoy receptor (sActRIIB-Fc). sActRIIB-Fc treatment resulted in significantly decreased LβT2 tumour volume. Reduced Smad2 phosphorylation as well as inhibition of tumour-induced FSH production confirmed the efficient targeting of activin-downstream signalling in treated tumours. More interestingly, treated tumours showed significantly fewer endothelial cells associated with reduced Vegfa expression. In vitro treatment of LβT2 cells with sActRIIB-Fc had no effect on cell proliferation or apoptosis, but Vegfa expression was inhibited, pointing to a likely paracrine effect of LβT2 cells on endothelial cells through activin-mediated Vegfa regulation. Further in vitro and in vivo studies are now needed to pinpoint the exact roles of activin signalling in these processes prior to translating these observations to the clinic.