Both male and female reproductive functions are impacted by altered gonadotrophin secretion and action, which may also influence the development of endocrine tumours. To ascertain if chronic hypersecretion of human chorionic gonadotropin (hCG) contributes to the development of gonadal tumours, double transgenic (TG) mice that overexpress hCGα- and β-subunits were analysed. By the age of two months, ovarian tumours with characteristics of teratomas developed with 100% penetrance. Teratomas were also seen in wild-type ovaries orthotopically transplanted into TG mice, demonstrating an endocrine/paracrine mechanism for the hCG-induced ovarian tumorigenesis. Both and experiments showed oocyte parthenogenetic activation in TG females. In addition, ovaries showed reduced ovulatory gene expression, inhibited ERK1/2 phosphorylation, and impaired cumulus cell expansion. Hence, persistently high endocrine hCG activity causes parthenogenetic activation and development of ovarian teratomas, along with altered follicle development and impaired ERK1/2 signalling, offering a novel mechanism associated with the molecular pathogenesis of ovarian teratomas.

中文翻译：

---

转基因小鼠绒毛膜促性腺激素升高诱导孤雌激活和卵巢畸胎瘤

男性和女性的生殖功能都受到促性腺激素分泌和作用改变的影响，这也可能影响内分泌肿瘤的发展。为了确定人绒毛膜促性腺激素 (hCG) 的慢性分泌过多是否会导致性腺肿瘤的发生，对过度表达 hCGα 和 β 亚基的双转基因 (TG) 小鼠进行了分析。到两个月大时，具有畸胎瘤特征的卵巢肿瘤的外显率达到 100%。在原位移植到 TG 小鼠的野生型卵巢中也发现了畸胎瘤，这证明了 hCG 诱导卵巢肿瘤发生的内分泌/旁分泌机制。两项实验均显示 TG 雌性中卵母细胞孤雌生殖激活。此外，卵巢排卵基因表达减少，ERK1/2 磷酸化受到抑制，卵丘细胞扩张受损。因此，持续高的内分泌 hCG 活性会导致单性生殖激活和卵巢畸胎瘤的发展，以及卵泡发育的改变和 ERK1/2 信号传导受损，从而提供了与卵巢畸胎瘤分子发病机制相关的新机制。