Semaphorin 3B Gene Suppresses Tumor Growth Through the p53 Signaling Pathway and Neuropilin Receptors

Yan Ma, Mingming Fang, Xifa Zhou
{"title":"Semaphorin 3B Gene Suppresses Tumor Growth Through the p53 Signaling Pathway and Neuropilin Receptors","authors":"Yan Ma, Mingming Fang, Xifa Zhou","doi":"10.11648/j.ajcem.20170506.18","DOIUrl":null,"url":null,"abstract":"The semaphorin family has been demonstrated to possess tumor suppressor activity; semaphorin 3B (SEMA3B) is differentially expressed in several types of tumors, and has been identified as a tumor suppressor gene. SEMA3B is shown to be a target gene of p53, and it suppresses tumor growth through the p53 signaling pathway. The mechanisms underlying tumor suppression by SEMA3B include neuropilin receptors (NRP1 and NRP2), which reduce the action of vascular endothelial growth factor (VEGF), thus, inhibiting tumor angiogenesis. Deficiency or down-regulation of SEMA3B expression can be found in a variety of malignant tumors including lung cancer, ovarian cancer, nervous system tumors, and hepatobiliary tumors, and this suppression involves methylation, loss of heterozygosity (LOH) and enzyme cleavage. This review summarizes recent research approaches on the tumor suppression effects and mechanisms of SEMA3B.","PeriodicalId":404444,"journal":{"name":"American Journal of Clinical and Experimental Medicine","volume":"26 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2017-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"American Journal of Clinical and Experimental Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.11648/j.ajcem.20170506.18","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1

Abstract

The semaphorin family has been demonstrated to possess tumor suppressor activity; semaphorin 3B (SEMA3B) is differentially expressed in several types of tumors, and has been identified as a tumor suppressor gene. SEMA3B is shown to be a target gene of p53, and it suppresses tumor growth through the p53 signaling pathway. The mechanisms underlying tumor suppression by SEMA3B include neuropilin receptors (NRP1 and NRP2), which reduce the action of vascular endothelial growth factor (VEGF), thus, inhibiting tumor angiogenesis. Deficiency or down-regulation of SEMA3B expression can be found in a variety of malignant tumors including lung cancer, ovarian cancer, nervous system tumors, and hepatobiliary tumors, and this suppression involves methylation, loss of heterozygosity (LOH) and enzyme cleavage. This review summarizes recent research approaches on the tumor suppression effects and mechanisms of SEMA3B.
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
信号蛋白3B基因通过p53信号通路和Neuropilin受体抑制肿瘤生长
信号蛋白家族已被证明具有肿瘤抑制活性;信号蛋白3B (SEMA3B)在几种类型的肿瘤中存在差异表达,已被确定为肿瘤抑制基因。SEMA3B是p53的靶基因,通过p53信号通路抑制肿瘤生长。SEMA3B抑制肿瘤的机制包括神经匹林受体(NRP1和NRP2),它们降低血管内皮生长因子(VEGF)的作用,从而抑制肿瘤血管生成。在肺癌、卵巢癌、神经系统肿瘤、肝胆肿瘤等多种恶性肿瘤中均发现SEMA3B表达缺失或下调,这种抑制涉及甲基化、杂合性缺失(LOH)和酶裂解。本文就SEMA3B的抑瘤作用及其机制的研究进展进行综述。
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 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Comparing Olanzapine with Placebo in Patients with Anorexia Nervosa for Increasing BMI and Weight Gain On the Governance of the Basic Healthcare Security System and Economic Development in China in the Context of COVID-19 Retrospective Analysis of Three Different Methods for the Treatment of Macrolide-Unresponsive Mycoplasma Pneumoniae Pneumonia in Children Inflammatory Markers in the Diagnosis of Neonatal Necrotizing Enterocolitis Mechanism Study of GanDouLing Mitigating Liver Fibrosis in Wilson’s Disease via Regulating the PI3K/AKT/mTOR Pathway to Activate Autophagy
×
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