Suppr超能文献

胃饥饿素与胃肠道间质瘤

Ghrelin and gastrointestinal stromal tumors.

作者信息

Zhu Chang-Zhen, Liu Dong, Kang Wei-Ming, Yu Jian-Chun, Ma Zhi-Qiang, Ye Xin, Li Kang

机构信息

Chang-Zhen Zhu, Dong Liu, Wei-Ming Kang, Jian-Chun Yu, Zhi-Qiang Ma, Xin Ye, Kang Li, Department of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100730, China.

出版信息

World J Gastroenterol. 2017 Mar 14;23(10):1758-1763. doi: 10.3748/wjg.v23.i10.1758.

Abstract

Ghrelin, as a kind of multifunctional protein polypeptide, is mainly produced in the fundus of the stomach and can promote occurrence and development of many tumors, including gastrointestinal tumors, which has been proved by the relevant researches. Most gastrointestinal stromal tumors (GISTs, about 80%), as the most common mesenchymal tumor, also develop in the fundus. Scientific research has confirmed that ghrelin, its receptors and mRNA respectively can be found in GISTs, which demonstrated the existence of a ghrelin autocrine/paracrine loop in GIST tissues. However, no reports to date have specified the mechanism whether ghrelin can promote the occurrence and development of GISTs. Studies of pulmonary artery endothelial cells in a low-oxygen environment and cardiac muscle cells in an ischemic environment have shown that ghrelin can activate the phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway. Moreover, some studies of GISTs have confirmed that activation of the PI3K/AKT/mTOR pathway can indeed promote the growth and progression of GISTs. Whether ghrelin is involved in the development or progression of GISTs through certain pathways remains unknown. Can we find a new target for the treatment of GISTs? This review explores and summaries the relationship among ghrelin, the PI3K/AKT/mTOR pathway and the development of GISTs.

摘要

胃饥饿素作为一种多功能蛋白质多肽,主要在胃底产生,并且相关研究已证实它可促进包括胃肠道肿瘤在内的多种肿瘤的发生和发展。作为最常见的间叶组织肿瘤,大多数胃肠道间质瘤(GIST,约80%)也发生于胃底。科研已证实,在胃肠道间质瘤中可分别发现胃饥饿素、其受体及信使核糖核酸,这表明在胃肠道间质瘤组织中存在胃饥饿素自分泌/旁分泌环。然而,迄今为止尚无报道明确胃饥饿素促进胃肠道间质瘤发生和发展的机制。对低氧环境下肺动脉内皮细胞和缺血环境下心肌细胞的研究表明,胃饥饿素可激活磷脂酰肌醇3激酶/蛋白激酶B/雷帕霉素靶蛋白(PI3K/AKT/mTOR)信号通路。此外,一些对胃肠道间质瘤的研究已证实,PI3K/AKT/mTOR通路的激活确实可促进胃肠道间质瘤的生长和进展。胃饥饿素是否通过某些途径参与胃肠道间质瘤的发生或进展仍不清楚。我们能否找到治疗胃肠道间质瘤的新靶点?这篇综述探讨并总结了胃饥饿素、PI3K/AKT/mTOR通路与胃肠道间质瘤发生发展之间的关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab98/5352915/99a22e2ee31d/WJG-23-1758-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验