Department of Gynecology, Affiliated Hospital of Jining Medical University, Jining 272100, China.
Depatment of Obstetrics, Pingdu People's Hospital, Qingdao 266700, China.
J Healthc Eng. 2022 Jan 27;2022:8094385. doi: 10.1155/2022/8094385. eCollection 2022.
miR-206 was reported to be a tumor suppressor in bladder cancer. In this study, we explore the expression and function of miR-206 in endometriosis (EM).
40 EM patients undergoing total hysterectomy were selected as the experimental group. RT-qPCR assay was adopted to detect the expression of MALAT1 and miR-206 in EM. Cell proliferation was detected by EdU incorporation and colony formation assay. Cell migration and invasion viability of ESCs were examined by transwell assay and wound healing assay. Flow cytometry was carried out to assess cell apoptosis of ESCs. The protein expressions of Bcl-2 and Bax were examined by western blot assay. The relationship between miR-206 and MALAT1 was verified by the dual-luciferase reporter assay and RNA pull-down assay.
In this work, miR-206 was found to be downregulated in EM. Functional experiments displayed that miR-206 mimic repressed cell proliferation, migration, and invasion of ESCs and promoted cell apoptosis of ESCs. Furthermore, miR-206 mimic reduced the expression of Bcl-2 but enhanced the expression of Bax. MALAT1 was found to be upregulated in EM. Furthermore, MALAT1 was indicated to be a target of miR-206. Additionally, MALAT1 was found to alleviate the influence of miR-206 on cell progression of ESCs. Furthermore, miR-206 inhibited tumor growth .
This study indicated that miR-206 inhibited cell progression by regulating MALAT1 in EM. Hence, miR-206 was suggested to be a possible target for EM treatment.
miR-206 被报道为膀胱癌的肿瘤抑制因子。在这项研究中，我们探讨了 miR-206 在子宫内膜异位症（EM）中的表达和功能。
选择 40 例行全子宫切除术的 EM 患者作为实验组。采用 RT-qPCR 检测 EM 中 MALAT1 和 miR-206 的表达。通过 EdU 掺入和集落形成实验检测细胞增殖。通过 Transwell 实验和划痕愈合实验检测 ESC 的细胞迁移和侵袭活力。通过流式细胞术评估 ESC 的细胞凋亡。通过 Western blot 检测 Bcl-2 和 Bax 的蛋白表达。通过双荧光素酶报告实验和 RNA 下拉实验验证 miR-206 和 MALAT1 之间的关系。
在这项工作中，发现 miR-206 在 EM 中下调。功能实验显示，miR-206 模拟物抑制 ESC 的增殖、迁移和侵袭，并促进 ESC 的细胞凋亡。此外，miR-206 模拟物降低了 Bcl-2 的表达，但增强了 Bax 的表达。MALAT1 在 EM 中上调。此外，MALAT1 被表明是 miR-206 的靶标。此外，MALAT1 被发现减轻了 miR-206 对 ESC 细胞进展的影响。此外，miR-206 抑制肿瘤生长。
本研究表明，miR-206 通过调节 EM 中的 MALAT1 抑制细胞进展。因此，miR-206 被认为是 EM 治疗的一个可能靶点。
