靶向癌细胞与癌症相关成纤维细胞之间的代谢串扰
Targeting Metabolic Cross Talk Between Cancer Cells and Cancer-Associated Fibroblasts.
作者信息
Jung Jin G, Le Anne
机构信息
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Department of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
出版信息
Adv Exp Med Biol. 2021;1311:205-214. doi: 10.1007/978-3-030-65768-0_15.
Although cancer has classically been regarded as a genetic disease of uncontrolled cell growth, the importance of the tumor microenvironment (TME) [1, 2] is continuously emphasized by the accumulating evidence that cancer growth is not simply dependent on the cancer cells themselves [3, 4] but also dependent on angiogenesis [5-8], inflammation [9, 10], and the supporting roles of cancer-associated fibroblasts (CAFs) [11-13]. After the discovery that CAFs are able to remodel the tumor matrix within the TME and provide the nutrients and chemicals to promote cancer cell growth [14], many studies have aimed to uncover the cross talk between cancer cells and CAFs. Moreover, a new paradigm in cancer metabolism shows how cancer cells act like "metabolic parasites" to take up the high-energy metabolites, such as lactate, ketone bodies, free fatty acids, and glutamine from supporting cells, including CAFs and cancer-associated adipocytes (CAAs) [15, 16]. This chapter provides an overview of the metabolic coupling between CAFs and cancer cells to further define the therapeutic options to disrupt the CAF-cancer cell interactions.
尽管癌症传统上被视为一种细胞生长失控的基因疾病，但越来越多的证据不断强调肿瘤微环境（TME）的重要性，即癌症生长不仅依赖于癌细胞本身[3,4]，还依赖于血管生成[5-8]、炎症[9,10]以及癌症相关成纤维细胞（CAF）的支持作用[11-13]。在发现CAF能够重塑TME内的肿瘤基质并提供促进癌细胞生长的营养物质和化学物质后[14]，许多研究旨在揭示癌细胞与CAF之间的相互作用。此外，癌症代谢的新范式表明癌细胞如何像“代谢寄生虫”一样从包括CAF和癌症相关脂肪细胞（CAA）在内的支持细胞中摄取高能代谢物，如乳酸、酮体、游离脂肪酸和谷氨酰胺[15,16]。本章概述了CAF与癌细胞之间的代谢耦合，以进一步确定破坏CAF-癌细胞相互作用的治疗选择。
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