Liu Li, Yan Lu, Liao Ning, Wu Wan-Qin, Shi Jun-Ling
Key Laboratory for Space Bioscience and Biotechnology, School of Life Sciences, Northwestern Polytechnical University, 127 Youyi West Road, Xi'an 710072, China.
Cancers (Basel). 2020 Feb 4;12(2):352. doi: 10.3390/cancers12020352.
The difficulty of early diagnosis and the development of drug resistance are two major barriers to the successful treatment of cancer. Autophagy plays a crucial role in several cellular functions, and its dysregulation is associated with both tumorigenesis and drug resistance. Unc-51-like kinase 1 (ULK1) is a serine/threonine kinase that participates in the initiation of autophagy. Many studies have indicated that compounds that directly or indirectly target ULK1 could be used for tumor therapy. However, reports of the therapeutic effects of these compounds have come to conflicting conclusions. In this work, we reviewed recent studies related to the effects of ULK1 on the regulation of autophagy and the development of drug resistance in cancers, with the aim of clarifying the mechanistic underpinnings of this therapeutic target.
早期诊断的困难和耐药性的产生是癌症成功治疗的两大主要障碍。自噬在多种细胞功能中起着关键作用,其失调与肿瘤发生和耐药性均相关。Unc-51样激酶1(ULK1)是一种参与自噬起始的丝氨酸/苏氨酸激酶。许多研究表明,直接或间接靶向ULK1的化合物可用于肿瘤治疗。然而,关于这些化合物治疗效果的报道得出了相互矛盾的结论。在这项工作中,我们综述了近期有关ULK1对癌症中自噬调节和耐药性发展影响的研究,旨在阐明这一治疗靶点的作用机制。