Pelvic Floor and Postpartum Rehabilitation Center, Changsha Maternal and Child Health Care Hospital, Changsha, Hunan 410007, PR China.
Department of Gynaecology, Changsha Maternal and Child Health Care Hospital, Changsha, Hunan 410007, PR China.
Reprod Biol. 2022 Sep;22(3):100675. doi: 10.1016/j.repbio.2022.100675. Epub 2022 Jul 25.
MALAT1, microRNA (miR)-142-3p, and CXCR7 are critical molecules mediating endometriosis progression, and their correlation in endometriosis has been barely discussed. Thus, this research sought to survey the impact of MALAT1 on endometrial stromal cell (ESC) proliferation, apoptosis, and inflammation via miR-142-3p/CXCR7 axis to promote explorations on endometriosis. In endometrial tissues and ESCs, CXCR7 expression was determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot analysis and miR-142-3p and MALAT1 expression by qRT-PCR. Then, ESC proliferation was assessed by CCK-8 and EdU labeling assays, apoptosis by flow cytometry, and levels of inflammatory factors tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in ESC supernatant by enzyme linked immunosorbent assay. The interactions among CXCR7, miR-142-3p, and MALAT1 were evaluated by dual luciferase reporter gene, RNA pull-down, and Argonaute 2- RNA immunoprecipitation assays. At last, the relevance of miR-142-3p to MALAT1 and that of miR-142-3p to CXCR7 in ectopic endometrial tissues were analyzed using Pearson correlation analysis. CXCR7 and MALAT1 were overexpressed whilst miR-142-3p was lowly expressed in ectopic endometrial tissues. CXCR7 silencing or miR-142-3p overexpression reduced proliferative ability and enhanced apoptosis rate in ESCs and decreased TNF-α, IL-1β, and IL-6 levels in cell supernatant. miR-142-3p negatively targeted CXCR7 while MALAT1 negatively targeted miR-142-3p. However, MALAT1 silencing diminished ESC proliferation and TNF-α, IL-1β, and IL-6 levels in ESC supernatant and elevated ESC apoptosis, which was counterweighed by inhibiting miR-142-3p. Conclusively, MALAT1 promoted ESC proliferation and inflammatory factor expression and inhibited ESC apoptosis via miR-142-3p/CXCR axis.
MALAT1、microRNA（miR）-142-3p 和 CXCR7 是介导子宫内膜异位症进展的关键分子，它们在子宫内膜异位症中的相关性几乎没有被讨论过。因此，本研究旨在通过 miR-142-3p/CXCR7 轴调查 MALAT1 对子宫内膜基质细胞（ESC）增殖、凋亡和炎症的影响，以促进对子宫内膜异位症的研究。通过定量逆转录聚合酶链反应（qRT-PCR）和 Western blot 分析检测子宫内膜组织和 ESC 中的 CXCR7 表达，通过 qRT-PCR 检测 miR-142-3p 和 MALAT1 表达。然后，通过 CCK-8 和 EdU 标记测定 ESC 增殖，通过流式细胞术测定凋亡，通过酶联免疫吸附测定法测定 ESC 上清液中肿瘤坏死因子（TNF）-α、白细胞介素（IL）-1β 和 IL-6 等炎症因子的水平。通过双荧光素酶报告基因、RNA 下拉和 Argonaute 2-RNA 免疫沉淀测定评估 CXCR7、miR-142-3p 和 MALAT1 之间的相互作用。最后，通过 Pearson 相关性分析分析 miR-142-3p 与 MALAT1 以及 miR-142-3p 与异位子宫内膜组织中 CXCR7 的相关性。在异位子宫内膜组织中，CXCR7 和 MALAT1 表达上调，而 miR-142-3p 表达下调。沉默 CXCR7 或过表达 miR-142-3p 可降低 ESC 的增殖能力并增加 ESC 的凋亡率，同时降低细胞上清液中 TNF-α、IL-1β 和 IL-6 的水平。miR-142-3p 靶向 CXCR7，而 MALAT1 靶向 miR-142-3p。然而，沉默 MALAT1 可降低 ESC 的增殖能力和 ESC 上清液中 TNF-α、IL-1β 和 IL-6 的水平，并增加 ESC 凋亡，而抑制 miR-142-3p 则可逆转这种作用。综上所述，MALAT1 通过 miR-142-3p/CXCR 轴促进 ESC 增殖和炎症因子表达，并抑制 ESC 凋亡。
