The role of semaphorins and their receptors in gliomas.

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2012-09-23 DOI:10.1155/2012/902854
Janice Wai Sze Law, Alan Yiu Wah Lee
{"title":"The role of semaphorins and their receptors in gliomas.","authors":"Janice Wai Sze Law,&nbsp;Alan Yiu Wah Lee","doi":"10.1155/2012/902854","DOIUrl":null,"url":null,"abstract":"<p><p>Gliomas are the most common tumor in the central nervous system. High-grade glioblastomas are characterized by their high invasiveness and resistance to radiotherapy, leading to high recurrence rate and short median survival despite radical surgical resection. Characterizations of gliomas at molecular level have revealed aberrations of various growth factor receptors, receptor tyrosine kinases, and tumor suppressor genes that lead to deregulation of multiple signaling pathways, thereby contributing to abnormal proliferation, invasion, and resistance to apoptosis in cancer cells. Recently, accumulating evidence points to the emerging role of axon guidance molecules in glioma progression. Notably, many signaling events harnessed by guidance molecules to regulate cell migration and axon navigation during development are also found to be involved in the modulation of deregulated pathways in gliomas. This paper focused on the signalings triggered by the guidance molecule semaphorins and their receptors plexins and neuropilins, and how their crosstalk with oncogenic pathways in gliomas might modulate cancer progression. The emerging role of semaphorins and plexins as tumor suppressors or oncogenes is also discussed.</p>","PeriodicalId":89176,"journal":{"name":"Journal of signal transduction","volume":"2012 ","pages":"902854"},"PeriodicalIF":0.0000,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/902854","citationCount":"23","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of signal transduction","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1155/2012/902854","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2012/9/23 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 23

Abstract

Gliomas are the most common tumor in the central nervous system. High-grade glioblastomas are characterized by their high invasiveness and resistance to radiotherapy, leading to high recurrence rate and short median survival despite radical surgical resection. Characterizations of gliomas at molecular level have revealed aberrations of various growth factor receptors, receptor tyrosine kinases, and tumor suppressor genes that lead to deregulation of multiple signaling pathways, thereby contributing to abnormal proliferation, invasion, and resistance to apoptosis in cancer cells. Recently, accumulating evidence points to the emerging role of axon guidance molecules in glioma progression. Notably, many signaling events harnessed by guidance molecules to regulate cell migration and axon navigation during development are also found to be involved in the modulation of deregulated pathways in gliomas. This paper focused on the signalings triggered by the guidance molecule semaphorins and their receptors plexins and neuropilins, and how their crosstalk with oncogenic pathways in gliomas might modulate cancer progression. The emerging role of semaphorins and plexins as tumor suppressors or oncogenes is also discussed.

Abstract Image

Abstract Image

信号素及其受体在胶质瘤中的作用。
胶质瘤是中枢神经系统最常见的肿瘤。高级别胶质母细胞瘤的特点是高侵袭性和耐放疗,导致高复发率和中位生存期短,尽管根治性手术切除。胶质瘤在分子水平上的特征揭示了各种生长因子受体、受体酪氨酸激酶和肿瘤抑制基因的畸变,导致多种信号通路的失调,从而导致癌细胞异常增殖、侵袭和对凋亡的抵抗。最近,越来越多的证据表明轴突引导分子在胶质瘤进展中的作用。值得注意的是,在发育过程中,许多由引导分子调节细胞迁移和轴突导航的信号事件也被发现参与了胶质瘤中失调通路的调节。本文重点研究了神经胶质瘤中信号素及其受体丛蛋白和神经匹林所引发的信号,以及它们与肿瘤发生通路的串扰如何调节肿瘤的进展。还讨论了信号蛋白和丛蛋白作为肿瘤抑制因子或癌基因的新作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信