Lan Luo, Jian-Jun Cao, Hui-Min Zhang, Kun Chen, Xing-Hua Liao and Kun Li*
Affiliated Hospital of Shandong Academy of Medical Sciences, ChinaFulltext PDF
Background: The treatment of uterine fibroids and the development of new drugs depend on a deeper understanding of the developmental mechanisms of uterine fibroids. Here, the role of ESR1 and miR-17 on the uterine fibroids cell proliferation and apoptosis and their relationship were investigated in USMCs. Methods: The CCK-8 and EDU experiments explored the effects of ESR1 and MiR-17-5p on the viability and proliferation of UMSC cell lines; TUNEI studied the effects of ESR1 and MiR-17- 5p on apoptosis of USMC cells, and WB detected ESR1 and MiR-17-5p expression of apoptosis marker gene; luciferase report experiment and WB explore the molecular mechanism of MiR-17- 5p inhibiting ESR1 expression and ESR1 promoting TP53 expression, CHIP experiment further explores the molecular mechanism of ESR1 promoting TP53 expression. Results: Our results showed that ESR1 increased the proliferation of USMCs and inhibited their apoptosis. In addition, ESR1 could directly bind the promoter region of TP53 and inhibit its expression. MiR-17 increased the apoptosis of USMCs and inhibited their proliferation via decreasing the level of ESR1 by targeting its 3’UTR. Conclusion: Finally, we concluded that MiR-17-5p regulates the proliferation and apoptosis of uterine fibroids by targeting ESR1
MiR-17-5p; Proliferation; Apoptosis; Uterine fibroids; ESR1
Luo L, Cao J-J, Zhang H-M, Chen K, Liao X-H, Li K. MiR-17-5p Regulates Proliferation and Apoptosis of Uterine Fibroids via Targeting ESR1. Clin Oncol. 2020; 5: 1724.