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自噬是以细胞内自噬体形成为特征,通过溶酶体吸收降解自身受损细胞器和大分子的一种自我消化过程,是细胞维持稳态的重要机制。自噬广泛参与多种重要的细胞功能,既能在代谢应激状态下保护受损细胞,又可能因为过度激活导致细胞发生II型程序性死亡,从而引发多种疾病,尤其对肿瘤的发生和发展更是发挥着“双刃剑”的作用。自噬通过多种分子信号机制调控肿瘤进程,包括mTOR依赖性和mTOR非依赖性途径。mTOR作为生长因子、能量和营养状态的感受器,可通过调节下游自噬复合物的形成,直接调控细胞自噬。阐明mTOR与细胞自噬的相互作用机制将有助于从分子水平上对各肿瘤病变进行分析和治疗。因此,本文就自噬与PI3K/Akt/mTOR通路在肿瘤中的研究进展作一综述。
Autophagy is characterized by the formation of intracellular autophagosomes, a self-digestion process that degrades its own damaged organelles and macromolecules via lysosomal uptake, and is an important mechanism by which cells maintain homeostasis. A wide range of autophagy involved in a variety of important cellular functions, both in metabolic stress protection of damaged cells, but also may be due to over-activation of cells to cause type II programmed death, which led to a variety of diseases, especially for the occurrence of tumors and Development is even playing a “double-edged sword” role. Autophagy regulates tumor progression through a variety of molecular signaling mechanisms, including mTOR-dependent and mTOR-independent pathways. As a growth factor, energy and nutrient receptor, mTOR directly regulates autophagy by regulating the formation of downstream autophagy complexes. The elucidation of the mechanism of mTOR and autophagy interaction will help the analysis and treatment of tumor lesions at the molecular level. Therefore, the progress of autophagy and PI3K / Akt / mTOR pathway in tumors is reviewed in this article.