Two-sided role of estrogen on endometrial carcinogenesis: stimulator or suppressor?

Endometrial carcinoma (EC) often expresses estrogen receptors (ER), and the growth of EC is stimulated by estrogen. Therefore, EC is considered to be an estrogen-dependent tumor. However, the role of estrogen in endometrial carcinogenesis is somewhat unclear because the majority of EC occurs at peri- or post menopause when serum estrogen levels are generally decreased. In this article, we describe the double-edged role of estrogen in the genesis of EC, especially in terms of mismatch repair functions <i>in vitro</i> and <i>in vivo</i>, i.e. when serum estradiol (E2) levels are relatively low (approximately less than 90 pg/ml), and E2 enhance the carcinogenesis, whereas high E2 levels may suppress the carcinogenesis. This will deepen mechanistic insight into unopposed estrogen.

子宫内膜癌（Endometrial carcinoma, EC）通常表达雌激素受体（Estrogen Receptors, ER），其生长可被雌激素刺激，因此EC被视为雌激素依赖性肿瘤。然而，由于绝大多数子宫内膜癌发生于围绝经期或绝经后阶段，此时血清雌激素水平普遍降低，因此雌激素在子宫内膜癌变过程中的具体作用仍存在一定模糊性。本文阐述了雌激素在子宫内膜癌发生发展中发挥的双刃剑作用，尤其从体外（in vitro）与体内（in vivo）层面聚焦错配修复功能的变化：当血清雌二醇（E2）水平相对较低（约低于90 pg/ml）时，E2可促进癌变进程；而当E2水平升高时，则可能抑制癌变发生。本研究将加深学界对非对抗性雌激素相关机制的认知。