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Updated: Feb 11, 2026

Preparation and In Vitro Characterization of Magnetized miR-modified Endothelial Cells
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Progesterone-Induced miR-145/miR-143 Inhibits the Proliferation of Endometrial Epithelial Cells

Dong-Zhi Yuan1, Yi Lei1, Dan Zhao1

  • 11 Department of Physiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, People's Republic of China.

Reproductive Sciences (Thousand Oaks, Calif.)
|April 18, 2018
PubMed

Our previous study showed that progesterone (P4) can specifically regulate the expression of some microRNAs (miRNAs) in endometrial epithelium. In the present study, we verified the P4-dependent expression of miR-145/miR-143 in endometrial epithelial cells, explored the regulative mechanism of the P4 receptor (PR), and investigated their effects on the proliferation of endometrial epithelial cells. Our results showed that P4 can induce the expression of miR-145/143 in endometrial epithelial cells by acting on the PR A subtype. P4-induced miR-145/143 can inhibit the expression of cyclin D2 by binding to cyclin D2 mRNA 3'UTR. It can also inhibit cell proliferation in mouse endometrial epithelium by arresting the cell cycle during the G1-S checkpoint. Furthermore, miR-145 and miR-143 can inhibit the proliferation of human endometrial cancer cells. In conclusion, P4-induced miR-145/miR-143 is an important regulator in the proliferation of endometrial epithelial cells, and it can also inhibit the proliferation of human endometrial cancer cells. Our study indicates miRNAs are important mechanism of P4 in inhibiting the proliferation of endometrial epithelial cells. And these miRNAs are potential candidates for the diagnosis of endometrial cancer and therapeutic targets.

Keywords:
cell cyclecyclin D2endometrial epithelial cellsmiR-145/miR-143progesterone (P4)

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