首页> 美国卫生研究院文献>Oncotarget >The sweet trap in tumors: aerobic glycolysis and potential targets for therapy
【2h】

The sweet trap in tumors: aerobic glycolysis and potential targets for therapy

机译:肿瘤中的甜蜜陷阱:有氧糖酵解和潜在的治疗靶标

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Metabolic change is one of the hallmarks of tumor, which has recently attracted a great of attention. One of main metabolic characteristics of tumor cells is the high level of glycolysis even in the presence of oxygen, known as aerobic glycolysis or the Warburg effect. The energy production is much less in glycolysis pathway than that in tricarboxylic acid cycle. The molecular mechanism of a high glycolytic flux in tumor cells remains unclear. A large amount of intermediates derived from glycolytic pathway could meet the biosynthetic requirements of the proliferating cells. Hypoxia-induced HIF-1α, PI3K-Akt-mTOR signaling pathway, and many other factors, such as oncogene activation and tumor suppressor inactivation, drive cancer cells to favor glycolysis over mitochondrial oxidation. Several small molecules targeting glycolytic pathway exhibit promising anticancer activity both in vitro and in vivo. In this review, we will focus on the latest progress in the regulation of aerobic glycolysis and discuss the potential targets for the tumor therapy.
机译:代谢变化是肿瘤的标志之一,近来引起了极大的关注。肿瘤细胞的主要代谢特征之一是即使在存在氧气的情况下也具有高水平的糖酵解作用,称为有氧糖酵解或Warburg效应。糖酵解途径的能量产生远少于三羧酸循环的能量产生。肿瘤细胞中高糖酵解通量的分子机制仍不清楚。来自糖酵解途径的大量中间体可以满足增殖细胞的生物合成需求。缺氧诱导的HIF-1α,PI3K-Akt-mTOR信号传导途径以及许多其他因素,例如致癌基因激活和肿瘤抑制因子失活,驱使癌细胞倾向于糖酵解而不是线粒体氧化。靶向糖酵解途径的几种小分子在体外和体内均显示出有希望的抗癌活性。在这篇综述中,我们将关注有氧糖酵解调控的最新进展,并讨论肿瘤治疗的潜在目标。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号