Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 823, Issue -, Pages 58-64Publisher
ELSEVIER
DOI: 10.1016/j.ejphar.2018.01.031
Keywords
aspirin; autophagy; hepatocellular carcinoma cells; Beclin-1; AMP-activated protein kinase; mammalian target of rapamycin
Categories
Funding
- National Natural Science Foundation of China [81570259, 81400234]
- Science and Technology Planning Project of Guangdong Province, China [2014A020212327, 2016A020215163]
- Elite Programme of The Second Affiliated Hospital of Guangzhou Medical University [52010205-035]
Ask authors/readers for more resources
Aspirin not only reduces the incidence of hepatocellular carcinoma (HCC) but also plays a synergistic role with chemotherapy for HCC treatment. However, the underlying mechanisms remain incompletely elucidated. Given that autophagy triggers cancer cell death, the present study examined the autophagic effect of aspirin on HCC cells. Results showed that aspirin increased LC3II/LC3I ratio, decreased p62 expression, and enhanced autophagic flux (autophagosome and autolysosome puncta) in Hep3B, HepG2, or SMMC-7721 cells, reflecting the autophagy of HCC cells. The autophagic effects of aspirin depended on Beclin-1 expression. Aspirin disrupted the interaction between Bcl-2 and Beclin-1. In addition to activating the AMP-activated protein kinase, c-Jun N-terminal kinase, and Glycogen synthase kinase-3 pathways, aspirin inhibited the mammalian-target-of rapamycin- S6K1/4E-BP1 signaling. Aspirin induced autophagy of HCC cell. This study contributes to understanding the chemoprotective and inhibitory effects of aspirin on HCC development.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available