Zhang Panpan, Cheng Shanshan, Sheng Xiaonan, Dai Huijuan, He Kang, Du Yueyao
Department of Gynecology and Obstetrics, Shanghai Key Laboratory of Gynecology Oncology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.
Department of Breast Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, No. 1630 Dongfang Road, Shanghai 200127, China.
Genes Dis. 2021 Dec 3;10(2):447-456. doi: 10.1016/j.gendis.2021.10.010. eCollection 2023 Mar.
Autophagy, as a special programmed cell death, is a critical degradative process that eliminates intracellular abnormal proteins or damage organelles to balance cell energy and favor cell metabolism with autophagy-related (ATG) proteins. Autophagy activation is being increasingly recognized as an essential hallmark in tumorigenesis through influencing the metabolism of stromal cells in the tumor microenvironment (TME) which comprises of tumor cells, cancer-associated fibroblasts (CAFs), cancer-associated endothelial cells (CAEs), immune cells and adipocytes. Tumor cells can reuse autophagy-involved recycling to maintain mitochondrial function and energy supply to meet the metabolic demand of their growth and proliferation. However, the mechanism through which autophagy can promote a crosstalk between tumor and stroma cells is not clear. Reprogramed metabolism is one of the main characteristics of TME leading to higher adaptability of tumor cells with diverse mechanisms. The activation of autophagy has expanded our understanding on the interaction between tumor metabolism and TME. The aim of this review is to report recent advances on the metabolic cross-talk between stromal cells and solid tumor cells induced by autophagy in TME and revealed potential therapeutic targets.
自噬作为一种特殊的程序性细胞死亡，是一个关键的降解过程，它通过自噬相关（ATG）蛋白消除细胞内异常蛋白质或受损细胞器，以平衡细胞能量并促进细胞代谢。自噬激活越来越被认为是肿瘤发生的一个重要标志，它通过影响肿瘤微环境（TME）中基质细胞的代谢来实现，肿瘤微环境由肿瘤细胞、癌症相关成纤维细胞（CAF）、癌症相关内皮细胞（CAE）、免疫细胞和脂肪细胞组成。肿瘤细胞可以利用自噬参与的循环来维持线粒体功能和能量供应，以满足其生长和增殖的代谢需求。然而，自噬促进肿瘤细胞与基质细胞之间相互作用的机制尚不清楚。代谢重编程是肿瘤微环境的主要特征之一，它通过多种机制使肿瘤细胞具有更高的适应性。自噬的激活扩展了我们对肿瘤代谢与肿瘤微环境之间相互作用的理解。本综述的目的是报告肿瘤微环境中自噬诱导的基质细胞与实体瘤细胞之间代谢相互作用的最新进展，并揭示潜在的治疗靶点。
