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miR-340-FHL2 轴抑制卵巢癌细胞生长和转移。

miR-340-FHL2 axis inhibits cell growth and metastasis in ovarian cancer.

机构信息

Institute of Genomic Medicine, Wenzhou Medical University, 325000, Wenzhou, Zhejiang, P. R. China.

Department of Obstetrics and Gynecology, The Second Affiliated Hospital and Yuying Children of Wenzhou Medical University, 325027, Wenzhou, Zhejiang, P. R. China.

出版信息

Cell Death Dis. 2019 May 8;10(5):372. doi: 10.1038/s41419-019-1604-3.

DOI:10.1038/s41419-019-1604-3
PMID:31068580
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6506554/
Abstract

Although increasing evidence indicated that deregulation of microRNAs (miRNAs) contributed to tumor initiation and progression, but little is known about the biological role of miR-340 in ovarian cancer (OC). In this study, we found that miR-340 expression was downregulated in OC tissues compared with its expression in normal ovarian epithelium and endometrium, and treatment with 5-aza-2'-deoxycytidine (5-Aza-dC) or trichostatin A (TSA) increased miR-340 expression in OC cells. In addition, ectopic miR-340 expression inhibited OC cell growth and metastasis in vitro and in vivo. Four and a half LIM domains protein 2 (FHL2) was confirmed as a direct target of miR-340 and silencing FHL2 mimicked the effects of miR-340 in OC cells. Further mechanistic study showed that miR-340 inhibited the Wnt/β-catenin pathway by targeting FHL2, as well as downstream cell cycle and epithelial-to-mesenchymal transition (EMT) signals in OC cells. Moreover, the greatest association between miR-340 and FHL2 was found in 481 ovarian serous cystadenocarcinoma tissues via pan-cancer analysis. Finally, we revealed that lower miR-340 or higher FHL2 was associated with poor OC patient outcomes. Our findings indicate that the miR-340-FHL2 axis regulates Wnt/β-catenin signaling and is involved in tumorigenesis in OC. Therefore, manipulating the expression of miR-340 or its target genes is a potential strategy in OC therapy.

摘要

尽管越来越多的证据表明 microRNAs（miRNAs）的失调导致了肿瘤的发生和发展，但miR-340 在卵巢癌（OC）中的生物学作用知之甚少。在这项研究中，我们发现miR-340 在 OC 组织中的表达低于其在正常卵巢上皮和子宫内膜中的表达，并且用 5-氮杂-2'-脱氧胞苷（5-Aza-dC）或曲古抑菌素 A（TSA）处理可增加 OC 细胞中的 miR-340 表达。此外，异位 miR-340 表达抑制 OC 细胞的体外和体内生长和转移。四半 LIM 结构域蛋白 2（FHL2）被确认为 miR-340 的直接靶标，沉默 FHL2 可模拟 miR-340 在 OC 细胞中的作用。进一步的机制研究表明，miR-340 通过靶向 FHL2 抑制 Wnt/β-catenin 通路，以及 OC 细胞中的下游细胞周期和上皮-间充质转化（EMT）信号。此外，通过泛癌分析，在 481 例卵巢浆液性囊腺癌组织中发现 miR-340 和 FHL2 之间的最大关联。最后，我们揭示了较低的 miR-340 或较高的 FHL2 与 OC 患者预后不良相关。我们的研究结果表明，miR-340-FHL2 轴调节 Wnt/β-catenin 信号通路，参与 OC 的肿瘤发生。因此，操纵 miR-340 或其靶基因的表达可能是 OC 治疗的一种潜在策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/7cdf06d51af0/41419_2019_1604_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/551ce54cc458/41419_2019_1604_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/624d13089916/41419_2019_1604_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/e9fa6f31209e/41419_2019_1604_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/6ae72d272faa/41419_2019_1604_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/f89523339ea9/41419_2019_1604_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/a4eee07c1d9e/41419_2019_1604_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/f24067f8f264/41419_2019_1604_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/7cdf06d51af0/41419_2019_1604_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/551ce54cc458/41419_2019_1604_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/624d13089916/41419_2019_1604_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/e9fa6f31209e/41419_2019_1604_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/6ae72d272faa/41419_2019_1604_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/f89523339ea9/41419_2019_1604_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/a4eee07c1d9e/41419_2019_1604_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/f24067f8f264/41419_2019_1604_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fcb/6506554/7cdf06d51af0/41419_2019_1604_Fig8_HTML.jpg

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