Narciclasine induces autophagy‐dependent apoptosis in triple‐negative breast cancer cells by regulating the AMPK‐ULK1 axis

Content Provider	Scilit
Author	Cao, Chuan Huang, Wei Zhang, Nan Wu, Fengbo Xu, Ting Pan, Xiaoli Peng, Cheng Han, Bo
Copyright Year	2018
Description	Journal: Cell Proliferation Autophagy and apoptosis are major types of eukaryotic programmed cell death, and regulating these processes holds promise for treating cancers. In this study, we explored the regulation mechanisms of narciclasine to autophagy and apoptosis processes in triple‐negative breast cancer. Effects of narciclasine on proliferation, apoptosis, and autophagy of HCC‐1937 and MDA‐MB‐231 triple‐negative breast cancer (TNBC) cells were assessed using transmission electronic microscopy, flow cytometry following staining with Annexin V‐FITC and propidium iodide, RNA sequencing, real‐time PCR, and Western blotting. The ability of narciclasine to inhibit growth of human HCC1937 TNBC xenografts in mice was assessed, and potential mechanisms of inhibition were explored using immunohistochemistry. Narciclasine inhibited TNBC cell proliferation and induced autophagy‐dependent apoptosis in a dose‐dependent manner. These apoptotic effects could be reversed using autophagy inhibitors, including an AMPK inhibitor and ULK1 siRNA. Consistent with these in vitro results, narciclasine significantly inhibited TNBC tumour growth in mice by upregulating autophagy‐dependent apoptosis. Our findings suggest that narciclasine regulates the AMPK‐ULK1 signalling axis to promote autophagy‐dependent apoptosis, demonstrating therapeutic potential against TNBC.
Related Links	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6528917/pdf
e-ISSN	13652184
DOI	10.1111/cpr.12518
Journal	Cell Proliferation
Issue Number	6
Volume Number	51
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2018-08-28
Access Restriction	Open
Subject Keyword	Journal: Cell Proliferation
Content Type	Text
Resource Type	Article