A small-molecule activator induces ULK1-modulating autophagy-associated cell death in triple negative breast cancer. Issue 4 (3rd April 2017)

• Record Type: Journal Article
• Authors: Ouyang, Liang; Zhang, Lan; Fu, Leilei; Liu, Bo
• Is Part Of: Autophagy. Volume 13:Issue 4(2017)
• Page Start: 777
• Page End: 778
• Publication Date: 2017-04-03
• Subjects: autophagy -- autophagy-associated cell death (ACD) -- triple negative breast cancer (TNBC) -- ULK1 activator -- UNC-51-like kinase 1 (ULK1); Autophagic vacuoles -- Periodicals; Apoptosis -- Periodicals; Cell death -- Periodicals; Lysosomes -- Periodicals; Degeneration (Pathology) -- Periodicals; Autophagy -- Periodicals; Cell Death -- Periodicals; Lysosomes -- Periodicals; Periodicals; 571.936
• DOI: 10.1080/15548627.2017.1283470
• Languages: English
• ISSNs: 1554-8627

Abstract

ABSTRACT: ULK1 (unc-51 like autophagy activating kinase 1) is well known to be required to initiate the macroautophagy/autophagy process, and thus activation of ULK1-modulating autophagy/autophagy-associated cell death (ACD) may be a possible therapeutic strategy in triple negative breast cancer (TNBC). Here, our integrated The Cancer Genome Atlas (TCGA) data set, tissue microarray-based analyses and multiple biologic evaluations together demonstrate a new small-molecule activator of ULK1 for better understanding of how ULK1, the mammalian homolog of yeast Atg1, as a potential drug target can regulate ACD by the ULK complex (ULK1-ATG13-RB1CC1/FIP200-ATG101), as well as other possible ULK1 interactors, including ATF3, RAD21 and CASP3/caspase3 in TNBC. Moreover, such new inspiring findings may help us discover that this activator of ULK1 (LYN-1604) with its anti-tumor activity and ACD-modulating mechanisms can be further exploited as a small-molecule candidate drug for future TNBC therapy.