Department of Gynaecology and Obstetrics, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Cancer Biother Radiopharm. 2020 Nov;35(9):650-660. doi: 10.1089/cbr.2019.3259. Epub 2020 Mar 18.
MIAT (myocardial infarction-associated transcript) regulates cell proliferation, apoptosis, and metastasis in several cancers. In this study, the authors aimed to explore the role of MIAT in ovarian cancer. The expression of MIAT in ovarian cancer subtypes, normal human ovarian surface epithelial and ovarian cancer cell lines was measured by qualitative real-time polymerase chain reaction (qRT-PCR). OVCAR3 and SKOV3 cells were transfected with MIAT overexpression plasmid or siMIAT. The cell growth ability was then evaluated by CCK-8 and colony formation assays. The cell migration and invasion rate were separately measured by wound-healing and transwell assays. The levels of epithelial-mesenchymal transition (EMT)-associated markers were evaluated by Western blotting. MIAT sponging miR-150-5p was predicted by starBase and confirmed by dual-luciferase reporter assays. The expression of miR-150-5p in OVCAR3 and SKOV3 cells with MIAT overexpression or knockdown, and in ovarian cancer subtypes was also measured by qRT-PCR. Further analyses confirmed the role of MIAT sponging miR-150-5p in ovarian cancer cells. MIAT was highly expressed in mesenchymal subtype ovarian cancer tissues and ovarian cancer cells. In OVCAR3 and SKOV3 cells, overexpression of MIAT promoted, and knockdown of MIAT suppressed the cell growth, migration, invasion, and EMT. miR-150-5p was sponged and regulated by MIAT. miR-150-5p was downregulated in mesenchymal subtype ovarian cancer. Suppression of cell migration, invasion, and EMT caused by miR-150-5p overexpression was rescued by MIAT overexpression. MIAT acts as an oncogene in ovarian cancer cells through sponging miR-150-5p. MIAT or miR-150-5p expression might be a potential prognostic biomarker for ovarian cancer patients. MIAT and miR-150-5p are potential therapeutic targets in treatment of ovarian cancer.
MIAT（心肌梗死相关转录物）在几种癌症中调节细胞增殖、凋亡和转移。在这项研究中，作者旨在探讨 MIAT 在卵巢癌中的作用。通过定性实时聚合酶链反应（qRT-PCR）测量卵巢癌亚型、正常人类卵巢表面上皮和卵巢癌细胞系中的 MIAT 表达。用 MIAT 过表达质粒或 siMIAT 转染 OVCAR3 和 SKOV3 细胞。然后通过 CCK-8 和集落形成测定评估细胞生长能力。通过划痕愈合和 Transwell 测定分别测量细胞迁移和侵袭率。通过 Western blot 评估上皮-间充质转化（EMT）相关标志物的水平。通过 starBase 预测并通过双荧光素酶报告基因测定证实 MIAT 海绵 miR-150-5p。通过 qRT-PCR 测量具有 MIAT 过表达或敲低的 OVCAR3 和 SKOV3 细胞以及卵巢癌亚型中的 miR-150-5p 表达。进一步的分析证实了 MIAT 海绵 miR-150-5p 在卵巢癌细胞中的作用。MIAT 在间充质亚型卵巢癌组织和卵巢癌细胞中高表达。在 OVCAR3 和 SKOV3 细胞中，MIAT 的过表达促进了细胞生长、迁移、侵袭和 EMT，而 MIAT 的敲低则抑制了这些过程。miR-150-5p 被 MIAT 海绵吸附并调节。miR-150-5p 在间充质亚型卵巢癌中下调。miR-150-5p 过表达引起的细胞迁移、侵袭和 EMT 抑制被 MIAT 过表达挽救。MIAT 通过海绵吸附 miR-150-5p 在卵巢癌细胞中发挥癌基因作用。MIAT 或 miR-150-5p 的表达可能是卵巢癌患者的潜在预后生物标志物。MIAT 和 miR-150-5p 是治疗卵巢癌的潜在治疗靶点。
