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Review
. 2020 Feb 4;12(2):352.
doi: 10.3390/cancers12020352.

A Review of ULK1-Mediated Autophagy in Drug Resistance of Cancer

Li Liu  1 , Lu Yan  1 , Ning Liao  1 , Wan-Qin Wu  1 , Jun-Ling Shi  1
Affiliations
Review

A Review of ULK1-Mediated Autophagy in Drug Resistance of Cancer

Li Liu et al. Cancers (Basel). .

Abstract

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.

Keywords: ULK1; autophagy; cancer; drug resistance.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Structure and biological function of ULK1. The domain of ULK1 contains three units including a kinase domain (KD), proline/serine-rich (PS) region, and C-terminal domain (CTD). AMPK and mTORC1 are upstream kinases that regulate ULK1. ATF4 is an activating transcription factor that directly regulates transcription of ULK1.
Figure 2
Figure 2
Summary of the relationships between ULK1, autophagy, and cancer.
Figure 3
Figure 3
A summary of how ULK1 is involved in the development of drug resistance in cancer.
See this image and copyright information in PMC

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