Metabolic phenotypes of cancer cells are heterogeneous and flexible as a tumor mass is a hurriedly evolving system capable of constant adaptation to oxygen and nutrient availability. The exact type of cancer metabolism arises from the combined effects of factors intrinsic to the cancer cells and factors proposed by the tumor microenvironment. As a result, a condition termed oncogenic metabolic symbiosis in which components of the tumor microenvironment (TME) promote tumor growth often occurs. Understanding how oncogenic metabolic symbiosis emerges and evolves is crucial for perceiving tumorigenesis. The process by which tumor cells reprogram their TME involves many mechanisms, including changes in intercellular communication, alterations in metabolic phenotypes of TME cells, and rearrangement of the extracellular matrix. It is possible that one molecule with a pleiotropic effect such as Caveolin‐1 may affect many of these pathways. Here, we discuss the significance of Caveolin‐1 in establishing metabolic symbiosis in TME.

中文翻译：

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Caveolin-1在致癌性代谢共生中。

癌细胞的代谢表型是异质的和灵活的，因为肿瘤块是一个能够不断适应氧气和养分利用率的快速发展的系统。癌症代谢的确切类型来自癌细胞固有的因素和肿瘤微环境提出的因素的综合作用。结果，经常发生称为致癌代谢共生的病症，其中肿瘤微环境（TME）的成分促进肿瘤生长。了解致癌性代谢共生如何发生和发展对于感知肿瘤发生至关重要。肿瘤细胞对其TME重新编程的过程涉及许多机制，包括细胞间通讯的改变，TME细胞代谢表型的改变以及细胞外基质的重排。一个具有多效作用的分子（例如Caveolin-1）可能会影响许多这些途径。在这里，我们讨论了Caveolin-1在TME中建立代谢共生的重要性。