受体酪氨酸激酶对自噬的调控及其研究进展*

自噬是真核生物进化上保守的溶酶体降解的生物学过程,在维护细胞内的稳态、消除有害组分等方面起到了重要作用。受体酪氨酸激酶家族(receptor tyrosine kinase,RTKs)是一类激酶蛋白,在正常细胞和癌症细胞的运动和侵袭中起着重要作用。RTKs蛋白既能促进自噬,也能抑制自噬。研究显示,RTKs能够在肿瘤和相关疾病中发挥自噬作用,比如表皮生长因子受体(epidermal growth factor receptor,EGFR)可以抑制自噬,从而促进肿瘤生长、增殖;还能通过RTK/Ras/ERK信号通路诱导自噬,进而参与诸如细胞免疫反应之类的相关疾病。主要综述了RTKs对自噬的调控作用和相关研究成果,为靶点靶向疗法的理论依据提供了基础。

Advances in the Regulation of Receptor Tyrosine Kinase on Autophagy

Autophagy is a very conservative biological process of lysosomal degradation in eukaryotic evolution, which plays an important role in maintaining cell homeostasis and eliminating harmful components. Receptor tyrosine kinases (RTKs) are a class of kinase proteins that play an important role in the movement and invasion of normal cells and cancer cells. RTKs protein can not only promote autophagy, but also inhibit autophagy. Studies have shown that RTKs can play a regulatory role in tumors and related diseases through autophagy. For example, epidermal growth factor receptor (EGFR) can inhibit autophagy, thereby promoting tumor growth and proliferation; it can also pass RTK/Ras/ERK signaling pathways to induce autophagy, which in turn participates in related diseases such as cellular immune responses. The regulatory effects of RTKs on autophagy and related research results, which provide a basis for the theoretical basis of target targeted therapy were reviewed.