Department of Physiology, Faculty of Medicine, Masaryk University, Brno, Czech Republic.
Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Brno, Czech Republic.
Int J Cancer. 2020 Oct 1;147(7):1793-1807. doi: 10.1002/ijc.32987. Epub 2020 Apr 21.
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.
癌细胞的代谢表型是异质且灵活的，因为肿瘤组织是一个快速进化的系统，能够不断适应氧气和营养物质的供应。确切的癌症代谢类型源自于癌细胞内在因素和肿瘤微环境提出的因素的综合作用。因此，肿瘤微环境（TME）中的成分促进肿瘤生长的一种称为致癌代谢共生的情况经常发生。理解致癌代谢共生的出现和演变对于理解肿瘤发生至关重要。肿瘤细胞重新编程其 TME 的过程涉及许多机制，包括细胞间通讯的变化、TME 细胞代谢表型的改变以及细胞外基质的重排。具有多效性效应的一种分子（如窖蛋白-1）可能会影响许多这些途径。在这里，我们讨论了 Caveolin-1 在建立 TME 代谢共生中的意义。
