Treatment with progesterone attenuates proliferation of endometrial polyps (EP) via regulation of expression of miR-320b and its target gene, MCL1

Abstract

The mechanism underlying the pathogenesis of endometrial polyps (EP) remains unclear. Endocrinopathy can be corrected by counteracting the effect of oestrogenic stimulation with progesterone, and systemic administration of pregestational agents was shown to block the effect of estrogenic stimulation and reverse the process of excessive endometrial growth [1]. Progesterone is an essential factor involved in the development of endometrial receptivity, and it maintains the homeostasis of the female endocrine system by blocking the synthesis of gonadotropin in the hypothalamus [2]. Meanwhile, the expression of miR-320 is down-regulated in patients with breast cancer [3]. By increasing the expression of miR-320, progesterone may block the infiltration of cells from the trophectoderm and uterus. Progesterone has been shown to affect the expression of multiple