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类黄酮介导的肿瘤血管生成抑制:血管生成素-酪氨酸激酶/磷脂酰肌醇-3激酶/蛋白激酶B的作用

Flavonoid-Mediated Suppression of Tumor Angiogenesis: Roles of Ang-Tie/PI3K/AKT.

作者信息

Saini Shallu, Tuli Hardeep Singh, Saini Reena V, Saini Adesh K, Sak Katrin, Kaur Damandeep, Shahwan Moyad, Chauhan Ritu, Chauhan Abhishek

机构信息

Department of Bio-Sciences and Technology, Maharishi Markandeshwar Engineering College, Maharishi Markandeshwar (Deemed to Be University), Mullana, Ambala 133207, India.

NGO Praeventio, 50407 Tartu, Estonia.

出版信息

Pathophysiology. 2024 Oct 12;31(4):596-607. doi: 10.3390/pathophysiology31040043.

Abstract

Angiogenesis is a process involved in the formation of new blood capillaries from pre-existing ones. It is regulated by several anti-angiogenic molecules involved in tumor growth and metastasis. The endothelial angiopoietin Ang-Tie/PI3K/AKT growth receptor pathway is necessary for healthy vascular development. The activation of AKT is controlled by a multistep process involving phosphoinositide 3-kinase (PI3K). This article aims to provide an overview of the role and mechanism of the Ang-Tie/PI3K/AKT signaling pathways and the potential of flavonoids as anti-angiogenic drugs. Flavonoids have shown great potential in preventing angiogenesis by targeting signaling pathways and exhibit additional anti-cancer properties. Research studies have revealed that the currently available anti-angiogenic drugs do not meet the safety and efficacy standards for treating tumor growth. Phytocompounds have long been a valuable resource for the development of novel therapeutic drugs. This article explores recent findings explaining the role and mechanism of the Ang-Tie/PI3K/AKT signaling pathways, as well as the interaction of flavonoids with angiogenic signaling pathways as a novel therapeutic approach. Several investigations have shown that synergistic studies of natural phytocompounds have great potential to target these pathways to inhibit tumor growth. Therefore, flavonoid-based medications may offer a more effective synergistic strategy to treat cancer.

摘要

血管生成是一个从已有的血管形成新的毛细血管的过程。它受几种参与肿瘤生长和转移的抗血管生成分子调控。内皮血管生成素Ang-Tie/PI3K/AKT生长受体通路对健康的血管发育至关重要。AKT的激活由一个涉及磷酸肌醇3激酶(PI3K)的多步骤过程控制。本文旨在概述Ang-Tie/PI3K/AKT信号通路的作用和机制以及黄酮类化合物作为抗血管生成药物的潜力。黄酮类化合物通过靶向信号通路在预防血管生成方面显示出巨大潜力,并具有额外的抗癌特性。研究表明,目前可用的抗血管生成药物不符合治疗肿瘤生长的安全性和有效性标准。植物化合物长期以来一直是开发新型治疗药物的宝贵资源。本文探讨了近期的研究结果,这些结果解释了Ang-Tie/PI3K/AKT信号通路的作用和机制,以及黄酮类化合物与血管生成信号通路的相互作用作为一种新型治疗方法。几项研究表明,天然植物化合物的协同研究在靶向这些通路以抑制肿瘤生长方面具有巨大潜力。因此,基于黄酮类化合物的药物可能为治疗癌症提供一种更有效的协同策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/896f/11503374/e6716b7b642d/pathophysiology-31-00043-g003.jpg

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