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基于靶向PI3K/AKT/mTOR信号通路的天然化合物的抗癌药物发现

Anticancer Drug Discovery from Natural Compounds Targeting PI3K/AKT/mTOR Signaling Pathway.

作者信息

da Silva Manuele Figueiredo, Lins Arestides Alves, Gomes Midiane Correia, Marinho Washley Phyama de Jesus, de Araújo Rodrigo Santos Aquino, de Moura Ricardo Olimpio, Zhan Peng, Nascimento Igor José Dos Santos, da Silva-Júnior Edeildo Ferreira

机构信息

Research Group of Biological and Molecular Chemistry, Federal University of Alagoas, A.C. Simões campus, Institute of Chemistry and Biotechnology, Maceió, 57072-970, Brazil.

Drug Development and Synthesis Laboratory, Department of Pharmacy, State University of Paraíba, Campina Grande, 58429-500, Brazil.

出版信息

Curr Med Chem. 2024 Oct 10. doi: 10.2174/0109298673325229240928040758.

DOI:10.2174/0109298673325229240928040758
PMID:39390838
Abstract

The term cancer is used to describe a complex pathology characterized by the uncontrollable proliferation of cells, which displays a fast metastatic spread, being a disease with difficult treatment. In this context, Phosphatidylinositol 3-kinase (PI3K) represents a promising pathway to be inhibited, aiming to develop anticancer agents, since it performs a pivotal role in regulating essential cellular processes, including cell proliferation, growth, autophagy, and apoptosis. In parallel, natural compounds can effectively represent a therapeutic strategy to fight against malignant cells. Then, compounds derived from various plant sources, such as flavonoids, terpenoids, alkaloids, coumarins, and lignans, have exhibited remarkable in vitro and in vivo anticancer properties. This review focused in the exploration of natural products targeting the PI3K/AKT/m-TOR signaling pathway, demonstrating that these compounds could even further investigated to reveal novel and effective anticancer drugs in the future.

摘要

“癌症”一词用于描述一种复杂的病理状态,其特征是细胞不受控制地增殖,并呈现快速转移扩散,是一种难以治疗的疾病。在这种情况下,磷脂酰肌醇3激酶(PI3K)是一个有望被抑制的途径,旨在开发抗癌药物,因为它在调节包括细胞增殖、生长、自噬和凋亡在内的基本细胞过程中发挥着关键作用。同时,天然化合物可以有效地成为对抗恶性细胞的治疗策略。然后,来自各种植物来源的化合物,如黄酮类、萜类、生物碱、香豆素和木脂素,已在体外和体内表现出显著的抗癌特性。本综述着重探索靶向PI3K/AKT/m-TOR信号通路的天然产物,表明这些化合物未来甚至可以进一步研究以揭示新型有效的抗癌药物。

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本文引用的文献

1
Analysis of some flavonoids for inhibitory mechanism against cancer target phosphatidylinositol 3-kinase (PI3K) using computational tool.使用计算工具分析某些黄酮类化合物对癌症靶点磷脂酰肌醇3-激酶(PI3K)的抑制机制。
Front Pharmacol. 2023 Oct 13;14:1236173. doi: 10.3389/fphar.2023.1236173. eCollection 2023.
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PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer.PI3K/AKT/mTOR 信号转导通路与癌症的靶向治疗。
Mol Cancer. 2023 Aug 18;22(1):138. doi: 10.1186/s12943-023-01827-6.
3
The neuroprotective mechanisms of naringenin: Inhibition of apoptosis through the PI3K/AKT pathway after hypoxic-ischemic brain damage.
柚皮素的神经保护机制:在缺氧缺血性脑损伤后通过 PI3K/AKT 通路抑制细胞凋亡。
J Ethnopharmacol. 2024 Jan 10;318(Pt A):116941. doi: 10.1016/j.jep.2023.116941. Epub 2023 Jul 20.
4
Exploring N-myristoyltransferase as a promising drug target against parasitic neglected tropical diseases.探索 N-豆蔻酰转移酶作为抗寄生虫性被忽视热带病的有前途的药物靶点。
Eur J Med Chem. 2023 Oct 5;258:115550. doi: 10.1016/j.ejmech.2023.115550. Epub 2023 Jun 8.
5
Anticancer Potentials of the Lignan Magnolin: A Systematic Review.《芝麻脂素的抗癌潜力:系统评价》
Molecules. 2023 Apr 23;28(9):3671. doi: 10.3390/molecules28093671.
6
Sanguinarine inhibits melanoma invasion and migration by targeting the FAK/PI3K/AKT/mTOR signalling pathway.血根碱通过靶向 FAK/PI3K/AKT/mTOR 信号通路抑制黑色素瘤侵袭和迁移。
Pharm Biol. 2023 Dec;61(1):696-709. doi: 10.1080/13880209.2023.2200787.
7
Curcumin and Plumbagin Synergistically Target the PI3K/Akt/mTOR Pathway: A Prospective Role in Cancer Treatment.姜黄素和白花丹素协同靶向 PI3K/Akt/mTOR 通路:在癌症治疗中的潜在作用。
Int J Mol Sci. 2023 Apr 2;24(7):6651. doi: 10.3390/ijms24076651.
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Pan-cancer genomic analysis shows hemizygous PTEN loss tumors are associated with immune evasion and poor outcome.泛癌症基因组分析表明,PTEN 杂合性缺失肿瘤与免疫逃避和不良预后相关。
Sci Rep. 2023 Mar 28;13(1):5049. doi: 10.1038/s41598-023-31759-6.
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Recent progress in targeted therapy for non-small cell lung cancer.非小细胞肺癌靶向治疗的最新进展
Front Pharmacol. 2023 Feb 21;14:1125547. doi: 10.3389/fphar.2023.1125547. eCollection 2023.
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