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肿瘤相关成纤维细胞的代谢重编程:基质成纤维细胞的“奴役”。

Metabolic Reprogramming of Cancer Associated Fibroblasts: The Slavery of Stromal Fibroblasts.

机构信息

Department of Public Health, University of Naples Federico II, 80131 Naples, Italy.

Department of Molecular Medicine and Medical Biotechnology, University of Naples Federico II, 80131 Naples, Italy.

出版信息

Biomed Res Int. 2018 Jun 5;2018:6075403. doi: 10.1155/2018/6075403. eCollection 2018.

DOI:10.1155/2018/6075403
PMID:29967776
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6008683/
Abstract

Cancer associated fibroblasts (CAFs) are the main stromal cell type of solid tumour microenvironment and undergo an activation process associated with secretion of growth factors, cytokines, and paracrine interactions. One of the important features of solid tumours is the metabolic reprogramming that leads to changes of bioenergetics and biosynthesis in both tumour cells and CAFs. In particular, CAFs follow the evolution of tumour disease and acquire a catabolic phenotype: in tumour tissues, cancer cells and tumour microenvironment form a network where the crosstalk between cancer cells and CAFs is associated with cell metabolic reprogramming that contributes to CAFs activation, cancer growth, and progression and evasion from cancer therapies. In this regard, the study of CAFs metabolic reprogramming could contribute to better understand their activation process, the interaction between stroma, and cancer cells and could offer innovative tools for the development of new therapeutic strategies able to eradicate the protumorigenic activity of CAFs. Therefore, this review focuses on CAFs metabolic reprogramming associated with both differentiation process and cancer and stromal cells crosstalk. Finally, therapeutic responses and potential anticancer strategies targeting CAFs metabolic reprogramming are reviewed.

摘要

癌症相关成纤维细胞(CAFs)是实体瘤微环境中的主要基质细胞类型,经历与生长因子、细胞因子分泌和旁分泌相互作用相关的激活过程。实体瘤的一个重要特征是代谢重编程,导致肿瘤细胞和 CAFs 的生物能量学和生物合成发生变化。特别是,CAFs 随着肿瘤疾病的演变而获得分解代谢表型:在肿瘤组织中,癌细胞和肿瘤微环境形成网络,癌细胞和 CAFs 之间的串扰与细胞代谢重编程相关,这有助于 CAFs 的激活、癌症的生长和进展,并逃避癌症治疗。在这方面,研究 CAFs 的代谢重编程有助于更好地理解其激活过程、基质和癌细胞之间的相互作用,并为开发新的治疗策略提供创新工具,以消除 CAFs 的促肿瘤活性。因此,本综述重点关注与分化过程和癌症以及基质细胞串扰相关的 CAFs 代谢重编程。最后,综述了针对 CAFs 代谢重编程的治疗反应和潜在的抗癌策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a387/6008683/809702926ab5/BMRI2018-6075403.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a387/6008683/809702926ab5/BMRI2018-6075403.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a387/6008683/809702926ab5/BMRI2018-6075403.001.jpg

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