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miR-141-3p 通过靶向 KLF-12 影响子宫内膜基质细胞的凋亡和迁移。

miR-141-3p affects apoptosis and migration of endometrial stromal cells by targeting KLF-12.

机构信息

Department of Obstetrics and Gynecology, The Third Hospital of Hebei Medical University, 139 Ziqiang Road, Shijiazhuang, 050051, Hebei, People's Republic of China.

Department of Gynecology, Shijiazhuang First Hospital, Shijiazhuang, 050011, Hebei, People's Republic of China.

出版信息

Pflugers Arch. 2019 Aug;471(8):1055-1063. doi: 10.1007/s00424-019-02283-2. Epub 2019 May 25.

DOI:10.1007/s00424-019-02283-2
PMID:31129698
Abstract

Endometriosis is an estrogen-dependent disease that is characterized by pelvic pain and infertility. MicroRNAs have been shown to implicate in the progression of endometriosis. In our study, we used real-time PCR to evaluate the expression of miR-141-3p in endometrial samples. In addition, western blot analysis was used to assess the expression of Krüppel-like factor 12 (KLF-12). The proliferation and migration of ectopic endometrial stromal cells (ESCs) were determined by MTT assay and Transwell assay, respectively. Cell apoptosis was evaluated using a Cell Death Detection ELISA Plus kit. The results showed that miR-141-3p and KLF-12 were significantly different in paired ectopic and eutopic endometrial samples. miR-141-3p overexpression significantly restrained the proliferation and migration and promoted the apoptosis of ectopic ESCs, whereas a decreased level of miR-141-3p was associated with opposite results. Furthermore, dual-luciferase reporter assay confirmed that KLF-12 was a novel target of miR-141-3p, while it also decreased the effects of miR-141-3p on the proliferation, apoptosis, and migration of ectopic ESCs. Our data suggested that enhanced expression of miR-141-3p suppressed the proliferation and migration of ectopic ESCs and promoted their apoptosis via targeting KLF-12. Our results may provide a novel potential therapeutic target for the treatment of endometriosis.

摘要

子宫内膜异位症是一种雌激素依赖性疾病,其特征是盆腔疼痛和不孕。研究表明 microRNAs 参与了子宫内膜异位症的进展。在我们的研究中,我们使用实时 PCR 来评估 miR-141-3p 在子宫内膜样本中的表达。此外,还使用 Western blot 分析来评估 Krüppel 样因子 12 (KLF-12) 的表达。通过 MTT 测定和 Transwell 测定分别确定异位子宫内膜基质细胞 (ESCs) 的增殖和迁移。使用细胞死亡检测 ELISA 试剂盒评估细胞凋亡。结果表明,配对的异位和在位子宫内膜样本中 miR-141-3p 和 KLF-12 表达存在显著差异。miR-141-3p 的过表达显著抑制了异位 ESCs 的增殖和迁移,并促进了其凋亡,而 miR-141-3p 水平的降低则与之相反。此外,双荧光素酶报告基因实验证实 KLF-12 是 miR-141-3p 的一个新的靶基因,而它也降低了 miR-141-3p 对异位 ESCs 增殖、凋亡和迁移的影响。我们的数据表明,增强的 miR-141-3p 表达通过靶向 KLF-12 抑制了异位 ESCs 的增殖和迁移,并促进了其凋亡。我们的研究结果可能为子宫内膜异位症的治疗提供一个新的潜在治疗靶点。

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