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代谢劫持:癌细胞利用的生存策略?

Metabolic hijacking: A survival strategy cancer cells exploit?

机构信息

Department of Physiological Sciences, Stellenbosch University, Stellenbosch, Matieland 7602, South Africa.

Department of Physiological Sciences, Stellenbosch University, Stellenbosch, Matieland 7602, South Africa.

出版信息

Crit Rev Oncol Hematol. 2017 Jan;109:1-8. doi: 10.1016/j.critrevonc.2016.11.010. Epub 2016 Nov 21.

DOI:10.1016/j.critrevonc.2016.11.010
PMID:28010894
Abstract

The majority of human tumours are comprised of cancerous epithelial cells that coexist with a multitude of different cell types and extracellular matrix components creating the cancer microenvironment. Cancer-associated fibroblasts (CAFs) are the most abundant mesenchymal cell types present within most human carcinomas. Recent evidence suggests that nutrient deprived epithelial cancer cells are able to survive these conditions, as a result of their ability to undergo extensive metabolic reprogramming and exploit the metabolic capacities of surrounding CAFs. Although several studies support the role of CAFs in tumour progression and metastasis, the molecular mechanisms underlying this pro-tumourigenic interaction remains to be elucidated. This review will discuss the complex metabolic interaction that exists between epithelial cancer cells and CAF's: focussing primarily on their functional role in tumour progression, metastasis and chemotherapeutic resistance. Attempts are made at delineating the molecular mechanisms underlying this pro-tumourigenic interaction, and potential CAF-based targets are suggested.

摘要

大多数人类肿瘤由癌细胞和多种不同的细胞类型以及细胞外基质成分组成,形成肿瘤微环境。癌相关成纤维细胞(CAF)是大多数人类癌中最丰富的间质细胞类型。最近的证据表明,营养剥夺的上皮癌细胞能够在这些条件下存活,这是由于它们能够进行广泛的代谢重编程并利用周围 CAF 的代谢能力。尽管有几项研究支持 CAF 在肿瘤进展和转移中的作用,但这种促进肿瘤发生的相互作用的分子机制仍有待阐明。本文将讨论上皮癌细胞和 CAF 之间存在的复杂代谢相互作用:主要集中在它们在肿瘤进展、转移和化疗耐药中的功能作用。尝试描述这种促进肿瘤发生的相互作用的分子机制,并提出潜在的基于 CAF 的靶点。

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