Department of Gynecology, Affiliated Obstetrics and Gynecology Hospital of Nanjing Medical University, Nanjing Maternal and Child Health Care Hospital, Nanjing, Jiangsu 210004, P.R. China.
Department of General Surgery, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, Jiangsu 210008, P.R. China.
Int J Mol Med. 2018 Nov;42(5):2793-2800. doi: 10.3892/ijmm.2018.3840. Epub 2018 Aug 24.
Endometriosis is a benign disease, but has invasion and metastasis characteristics similar to malignant tumors. Clinically, it is a difficult problem of gynecological clinical treatment for its high recurrence rate. It has been confirmed that miR-363 was downregulated in endometriosis tissues and miR-363 overexpression inhibited the invasion ability of endometrial stromal cells (ESCs). In order to explore the potential mechanism of miR-363-reduced ESC migration and invasion progression, we sought to demonstrate the targeted mRNA expression levels of miR-363 through microarray, and performed cluster analysis to identify potential functions of these targeted genes in ESCs. The wound migration assay showed that there was an observable trend of cell migration potential decrease after transfection with hsa-miR-363. The qRT-PCR result showed that compared to miR-363 negative control cell group, miR-363 was upregulated 3,264.58-fold after miR-363 lentiviral transfection in miR-363 mimics group. The microarray data showed that compared to ESCs miR-363 negative control cell group, 249 genes were upregulated in ESCs miR-363 mimics cells group, and 139 genes were downregulated. Gene Ontology analysis and the pathway analysis data demonstrated that these target genes are mainly involved in cell migration, cell adhesion and invasion, proliferation, apoptosis, alteration of endometrial cells and some related signaling pathways. Our study explored the gene expression pattern after miR-363 overexpression, which could expand the insights into the miR-363 function and molecular mechanisms in endometriosis.
子宫内膜异位症是一种良性疾病，但具有类似于恶性肿瘤的侵袭和转移特征。临床上，由于其高复发率，它是妇科临床治疗的一个难题。已经证实 miR-363 在子宫内膜异位症组织中表达下调，过表达 miR-363 可抑制子宫内膜基质细胞（ESCs）的侵袭能力。为了探讨 miR-363 降低 ESC 迁移和侵袭进展的潜在机制，我们试图通过微阵列证明 miR-363 的靶向 mRNA 表达水平，并进行聚类分析以确定这些靶向基因在 ESCs 中的潜在功能。划痕迁移实验表明，转染 hsa-miR-363 后细胞迁移潜能明显下降。qRT-PCR 结果显示，与 miR-363 阴性对照细胞组相比，miR-363 模拟物组 miR-363 的表达上调了 3264.58 倍。微阵列数据显示，与 ESCs miR-363 阴性对照细胞组相比，ESCs miR-363 模拟物组中有 249 个基因上调，139 个基因下调。GO 分析和通路分析数据表明，这些靶基因主要参与细胞迁移、细胞黏附与侵袭、增殖、凋亡、子宫内膜细胞改变以及一些相关信号通路。本研究探讨了 miR-363 过表达后的基因表达模式，这可能扩展对 miR-363 在子宫内膜异位症中的功能和分子机制的认识。
