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胃癌干细胞:代谢重编程一瞥

Gastric Cancer Stem Cells: A Glimpse on Metabolic Reprogramming.

作者信息

Addeo Martina, Di Paola Giuseppina, Verma Henu Kumar, Laurino Simona, Russi Sabino, Zoppoli Pietro, Falco Geppino, Mazzone Pellegrino

机构信息

Istituto di Ricerche Genetiche Gaetano Salvatore Biogem Scarl, Ariano Irpino, Italy.

Department of Biology, University of Naples Federico II, Naples, Italy.

出版信息

Front Oncol. 2021 Jun 16;11:698394. doi: 10.3389/fonc.2021.698394. eCollection 2021.

DOI:10.3389/fonc.2021.698394
PMID:34249759
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8262334/
Abstract

Gastric cancer (GC) is one of the most widespread causes of cancer-related death worldwide. Recently, emerging implied that gastric cancer stem cells (GCSCs) play an important role in the initiation and progression of GC. This subpopulation comprises cells with several features, such as self-renewal capability, high proliferating rate, and ability to modify their metabolic program, which allow them to resist current anticancer therapies. Metabolic pathway intermediates play a pivotal role in regulating cell differentiation both in tumorigenesis and during normal development. Thus, the dysregulation of both anabolic and catabolic pathways constitutes a significant opportunity to target GCSCs in order to eradicate the tumor progression. In this review, we discuss the current knowledge about metabolic phenotype that supports GCSC proliferation and we overview the compounds that selectively target metabolic intermediates of CSCs that can be used as a strategy in cancer therapy.

摘要

胃癌(GC)是全球癌症相关死亡最普遍的原因之一。最近,新出现的证据表明,胃癌干细胞(GCSCs)在胃癌的发生和发展中起重要作用。这一亚群细胞具有多种特性,如自我更新能力、高增殖率以及改变其代谢程序的能力,这些特性使它们能够抵抗目前的抗癌治疗。代谢途径中间体在肿瘤发生和正常发育过程中调节细胞分化方面起着关键作用。因此,合成代谢和分解代谢途径的失调为靶向GCSCs以根除肿瘤进展提供了重要契机。在本综述中,我们讨论了支持GCSC增殖的代谢表型的现有知识,并概述了可选择性靶向CSCs代谢中间体的化合物,这些化合物可作为癌症治疗的一种策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfe4/8262334/4b29143e4d14/fonc-11-698394-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfe4/8262334/a54f05f6ba7f/fonc-11-698394-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfe4/8262334/9f333c803102/fonc-11-698394-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfe4/8262334/4b29143e4d14/fonc-11-698394-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfe4/8262334/a54f05f6ba7f/fonc-11-698394-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfe4/8262334/d372ab15aa6c/fonc-11-698394-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfe4/8262334/9f333c803102/fonc-11-698394-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfe4/8262334/4b29143e4d14/fonc-11-698394-g004.jpg

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本文引用的文献

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Front Endocrinol (Lausanne). 2021 Mar 22;12:627745. doi: 10.3389/fendo.2021.627745. eCollection 2021.
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Targeting cancer stem cells for reversing therapy resistance: mechanism, signaling, and prospective agents.靶向肿瘤干细胞逆转治疗抵抗:机制、信号通路和潜在药物。
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Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries.
高通量药物筛选显示,环吡酮胺可产生胃癌干细胞样细胞。
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Cyclophilin A Inhibitors Suppress Proliferation and Induce Apoptosis of MKN45 Gastric Cancer Stem-like Cells by Regulating CypA/CD147-Mediated Signaling Pathway.亲环素 A 抑制剂通过调节 CypA/CD147 介导的信号通路抑制 MKN45 胃癌干细胞样细胞的增殖并诱导其凋亡。
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Atorvastatin inhibits the proliferation of MKN45-derived gastric cancer stem cells in a mevalonate pathway-independent manner.阿托伐他汀以一种不依赖甲羟戊酸途径的方式抑制MKN45来源的胃癌干细胞的增殖。
Korean J Physiol Pharmacol. 2022 Sep 1;26(5):367-375. doi: 10.4196/kjpp.2022.26.5.367.
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