Department of Gynecology and Obstetrics, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052 Henan Province, China.
Biomed Res Int. 2022 Mar 26;2022:7663379. doi: 10.1155/2022/7663379. eCollection 2022.
EMs is a kind of benign disease with certain malignant behaviors. The adhesion, invasive growth, and angiogenesis of ectopic endometrial cells are the pathological basis of EMs occurrence, but its etiology and pathogenesis have not been completely illustrated yet. In our research, we aim to investigate the role of miR-363 in the pathogenesis of endometriosis. Real-time quantitative PCR was used to detect the expression of miR-363 before and after ESC/NSC transfection. CCK-8, flow cytometry, and transwell assay were used to detect the effect of the miR-363 expression on cell proliferation, apoptosis, and invasion. The effects of the miR-363 expression on the contents of Fas/APO-1 and ICAM-1 in cell culture supernatant were detected by ELISA. qRT-PCR and WB assay were used to detect the effects of the miR-363 expression on the mRNA and protein expression levels of ICAM-1, MMP-7, and VEGF in ESC. The increased expression of miR-363 could inhibit the proliferation and invasion of ESC, promote apoptosis, and inhibit the secretion of FAS/APO-1 and ICAM-1. The knockdown expression of miR-363 promoted proliferation and invasion of NSC, inhibited apoptosis, and promoted secretion of FAS/APO-1 and ICAM-1. VCAM-1, VEGF, and MMP-7 were detected in ESCs before transfection. The protein expression level was higher than that of NSCs. Compared with pretransfection, the protein levels of VCAM-1, VEGF, and MMP-7 in the M-363 group were significantly downregulated. The downregulated expression of miR-363 was associated with a stronger cell proliferation ability, a lower cell apoptosis rate, and a stronger ESC. Migration is associated with invasiveness, proliferation, angiogenesis, and immune escape. The low expression of miR-363 promotes endogenesis through posttranscriptional regulation of target genes VCAM-1, MMP-7, and VEGF. The differential expression of miR-363 between ESC and NSC may be an important factor in the many biological differences between ESC and NSC.
子宫内膜异位症(EMs)是一种具有一定恶性行为的良性疾病。异位子宫内膜细胞的黏附、侵袭性生长和血管生成是 EMs 发生的病理基础,但病因和发病机制尚未完全阐明。在我们的研究中,我们旨在研究 miR-363 在子宫内膜异位症发病机制中的作用。实时定量 PCR 用于检测 ESC/NSC 转染前后 miR-363 的表达。CCK-8、流式细胞术和 Transwell 分析用于检测 miR-363 表达对细胞增殖、凋亡和侵袭的影响。ELISA 检测 miR-363 表达对细胞培养上清液中 Fas/APO-1 和 ICAM-1 含量的影响。qRT-PCR 和 WB 检测 miR-363 表达对 ESC 中 ICAM-1、MMP-7 和 VEGF mRNA 和蛋白表达水平的影响。miR-363 表达增加可抑制 ESC 的增殖和侵袭,促进凋亡,并抑制 Fas/APO-1 和 ICAM-1 的分泌。miR-363 的敲低表达促进 NSC 的增殖和侵袭,抑制凋亡,并促进 Fas/APO-1 和 ICAM-1 的分泌。转染前检测 ESCs 中 VCAM-1、VEGF 和 MMP-7 的表达。蛋白质表达水平高于 NSCs。与转染前相比,M-363 组 VCAM-1、VEGF 和 MMP-7 的蛋白水平明显下调。miR-363 的下调表达与更强的细胞增殖能力、更低的细胞凋亡率以及更强的 ESC 迁移能力有关。侵袭、增殖、血管生成和免疫逃避。miR-363 的低表达通过靶基因 VCAM-1、MMP-7 和 VEGF 的转录后调节促进内源性发生。miR-363 在 ESC 和 NSC 之间的差异表达可能是 ESC 和 NSC 之间许多生物学差异的重要因素。