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

Abstract

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 in vitro and in vivo, 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.

摘要

子宫内膜癌(EC)常表达雌激素受体(ER), 其生长受雌激素刺激。因此, EC被认为是一种雌激素依赖性肿瘤。然而, 雌激素在正常子宫内膜癌变过程中的作用尚不清楚, 因为大多数EC发生在绝经前后, 此时血清雌激素水平普遍下降。在本文中,我们描述了雌激素在EC发生过程中的双刃剑作用, 特别是在体外和体内的错配修复功能方面,即当血清雌二醇(E2)水平相对较低(大约不到90 pg / ml)时, E2有致癌作用, 而高E2水平可能抑制其致癌作用。这将加深对雌激素致癌机制的认识。

The Chinese abstracts are translated by Prof. Dr. Xiangyan Ruan and her team: Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing 100026, China.

Keywords:

• Endometrial carcinoma
• estradiol
• mismatch repair
• next-generation sequencing
• carcinogenesis

Disclosure statement

No potential conflict of interest was reported by the authors.