从microRNA研究中获得子宫内膜异位症有希望的治疗靶点。

IF 1.2 4区 医学 Q3 PATHOLOGY Medical Molecular Morphology Pub Date : 2022-06-01 Epub Date: 2021-11-30 DOI:10.1007/s00795-021-00308-3
Kaei Nasu, Yoko Aoyagi, Ruofei Zhu, Mamiko Okamoto, Kentaro Kai, Yasushi Kawano
{"title":"从microRNA研究中获得子宫内膜异位症有希望的治疗靶点。","authors":"Kaei Nasu,&nbsp;Yoko Aoyagi,&nbsp;Ruofei Zhu,&nbsp;Mamiko Okamoto,&nbsp;Kentaro Kai,&nbsp;Yasushi Kawano","doi":"10.1007/s00795-021-00308-3","DOIUrl":null,"url":null,"abstract":"<p><p>Endometriosis is a benign tumor that affect 6-10% women of reproductive age. To date, it is suggested that the aberrant microRNA (miRNA) expressions play important roles in the pathogenesis of endometriosis. Reviewing the literature, we found nine overexpressed miRNAs, which were thoroughly investigated in the context of endometriotic tissues and cells. Most of the overexpressed miRNAs induced endometriosis-specific characteristics including inhibition of apoptosis and decidualization, upregulation of fibrogenesis, invasion, migration, cell proliferation, attachment to extracellular matrix, inflammation, and angiogenesis in the endometriotic cells. Then, we found that the downstream target molecules of these miRNAs, such as early growth response protein-1, extracellular signal-regulated kinase, matrix metallopeptidase 1, signal transducer and activator of transcription 3, cyclooxygenase-2, phosphoinositide 3-kinase, AKT, mammalian target of rapamycin, and vascular endothelial growth factor-A are promising for the therapeutic targets of endometriosis. Recent findings suggest that complex molecular mechanisms leading to development and progression of endometriosis by miRNAs may exist in endometriosis. The meticulous balance between tumorigenic miRNAs and tumoristatic miRNAs may destine the natural course and response to the surgical, medical, and hormonal treatments of this disease. Further investigations into endometriosis-associated miRNAs may elucidate the pathogenesis of endometriosis and help to develop novel therapeutics.</p>","PeriodicalId":18338,"journal":{"name":"Medical Molecular Morphology","volume":null,"pages":null},"PeriodicalIF":1.2000,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"Promising therapeutic targets of endometriosis obtained from microRNA studies.\",\"authors\":\"Kaei Nasu,&nbsp;Yoko Aoyagi,&nbsp;Ruofei Zhu,&nbsp;Mamiko Okamoto,&nbsp;Kentaro Kai,&nbsp;Yasushi Kawano\",\"doi\":\"10.1007/s00795-021-00308-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Endometriosis is a benign tumor that affect 6-10% women of reproductive age. To date, it is suggested that the aberrant microRNA (miRNA) expressions play important roles in the pathogenesis of endometriosis. Reviewing the literature, we found nine overexpressed miRNAs, which were thoroughly investigated in the context of endometriotic tissues and cells. Most of the overexpressed miRNAs induced endometriosis-specific characteristics including inhibition of apoptosis and decidualization, upregulation of fibrogenesis, invasion, migration, cell proliferation, attachment to extracellular matrix, inflammation, and angiogenesis in the endometriotic cells. Then, we found that the downstream target molecules of these miRNAs, such as early growth response protein-1, extracellular signal-regulated kinase, matrix metallopeptidase 1, signal transducer and activator of transcription 3, cyclooxygenase-2, phosphoinositide 3-kinase, AKT, mammalian target of rapamycin, and vascular endothelial growth factor-A are promising for the therapeutic targets of endometriosis. Recent findings suggest that complex molecular mechanisms leading to development and progression of endometriosis by miRNAs may exist in endometriosis. The meticulous balance between tumorigenic miRNAs and tumoristatic miRNAs may destine the natural course and response to the surgical, medical, and hormonal treatments of this disease. Further investigations into endometriosis-associated miRNAs may elucidate the pathogenesis of endometriosis and help to develop novel therapeutics.</p>\",\"PeriodicalId\":18338,\"journal\":{\"name\":\"Medical Molecular Morphology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.2000,\"publicationDate\":\"2022-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Medical Molecular Morphology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s00795-021-00308-3\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2021/11/30 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"PATHOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical Molecular Morphology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s00795-021-00308-3","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/11/30 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"PATHOLOGY","Score":null,"Total":0}
引用次数: 2

摘要

子宫内膜异位症是一种良性肿瘤,影响6-10%的育龄妇女。迄今为止,研究表明microRNA (miRNA)的异常表达在子宫内膜异位症的发病机制中起重要作用。回顾文献,我们发现了9个过表达的mirna,并在子宫内膜异位症组织和细胞中进行了深入的研究。大多数过表达的miRNAs诱导了子宫内膜异位症的特异性特征,包括抑制细胞凋亡和蜕膜化,上调子宫内膜异位症细胞的纤维生成、侵袭、迁移、细胞增殖、细胞外基质附着、炎症和血管生成。然后,我们发现这些mirna的下游靶点分子,如早期生长反应蛋白-1、细胞外信号调节激酶、基质金属肽酶1、信号转导和转录激活因子3、环氧化酶-2、磷酸肌肽3激酶、AKT、哺乳动物雷帕霉素靶点、血管内皮生长因子- a等都是子宫内膜异位症的治疗靶点。最近的研究表明,在子宫内膜异位症中可能存在复杂的分子机制,导致mirna的发生和发展。致瘤性mirna和致瘤性mirna之间的微妙平衡可能决定了这种疾病的自然病程和对手术、药物和激素治疗的反应。对子宫内膜异位症相关mirna的进一步研究可能有助于阐明子宫内膜异位症的发病机制,并有助于开发新的治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Promising therapeutic targets of endometriosis obtained from microRNA studies.

Endometriosis is a benign tumor that affect 6-10% women of reproductive age. To date, it is suggested that the aberrant microRNA (miRNA) expressions play important roles in the pathogenesis of endometriosis. Reviewing the literature, we found nine overexpressed miRNAs, which were thoroughly investigated in the context of endometriotic tissues and cells. Most of the overexpressed miRNAs induced endometriosis-specific characteristics including inhibition of apoptosis and decidualization, upregulation of fibrogenesis, invasion, migration, cell proliferation, attachment to extracellular matrix, inflammation, and angiogenesis in the endometriotic cells. Then, we found that the downstream target molecules of these miRNAs, such as early growth response protein-1, extracellular signal-regulated kinase, matrix metallopeptidase 1, signal transducer and activator of transcription 3, cyclooxygenase-2, phosphoinositide 3-kinase, AKT, mammalian target of rapamycin, and vascular endothelial growth factor-A are promising for the therapeutic targets of endometriosis. Recent findings suggest that complex molecular mechanisms leading to development and progression of endometriosis by miRNAs may exist in endometriosis. The meticulous balance between tumorigenic miRNAs and tumoristatic miRNAs may destine the natural course and response to the surgical, medical, and hormonal treatments of this disease. Further investigations into endometriosis-associated miRNAs may elucidate the pathogenesis of endometriosis and help to develop novel therapeutics.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Medical Molecular Morphology
Medical Molecular Morphology 医学-病理学
CiteScore
2.90
自引率
5.60%
发文量
30
审稿时长
>12 weeks
期刊介绍: Medical Molecular Morphology is an international forum for researchers in both basic and clinical medicine to present and discuss new research on the structural mechanisms and the processes of health and disease at the molecular level. The structures of molecules, organelles, cells, tissues, and organs determine their normal function. Disease is thus best understood in terms of structural changes in these different levels of biological organization, especially in molecules and molecular interactions as well as the cellular localization of chemical components. Medical Molecular Morphology welcomes articles on basic or clinical research in the fields of cell biology, molecular biology, and medical, veterinary, and dental sciences using techniques for structural research such as electron microscopy, confocal laser scanning microscopy, enzyme histochemistry, immunohistochemistry, radioautography, X-ray microanalysis, and in situ hybridization. Manuscripts submitted for publication must contain a statement to the effect that all human studies have been reviewed by the appropriate ethics committee and have therefore been performed in accordance with the ethical standards laid down in an appropriate version of the 1964 Declaration of Helsinki. It should also be stated clearly in the text that all persons gave their informed consent prior to their inclusion in the study. Details that might disclose the identity of the subjects under study should be omitted.
期刊最新文献
Leucine drives LAT1-related SNAIL upregulation in glucose-starved pancreatic cancer cells. P4HA2 involved in SLUG-associated EMT predicts poor prognosis of patients with KRAS-positive colorectal cancer. Vitamin D-metabolizing enzyme CYP24A1 affects oncogenic behaviors of oral squamous cell carcinoma and its prognostic implication. Monomorphic T-cell post-transplant lymphoproliferative disorder with features of HHV8-negative primary effusion lymphoma: an autopsy case and review of the literature. Primary hepatobiliary mucoepidermoid carcinoma: a case report and review of literature.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1