The role of usnic acid-induced apoptosis and autophagy in hepatocellular carcinoma

Usnic acid (UA) is a multifunctional bioactive lichen secondary metabolite with potential anti-cancer properties. Although the promising therapeutic effects of UA have been investigated in different cancer cell lines, the mechanism driving UA-induced cell death has yet to be elucidated. As the type...

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Bibliographic Details
Published in:Human & experimental toxicology 2019-02, Vol.38 (2), p.201-215
Main Authors: Yurdacan, B, Egeli, U, Eskiler, G Guney, Eryilmaz, IE, Cecener, G, Tunca, B
Format: Article
Language:English
Subjects:
Anticancer properties
Antineoplastic Agents - pharmacology
Apoptosis
Apoptosis - drug effects
Autophagy
Autophagy - drug effects
Benzofurans - pharmacology
Biotechnology
Cancer
Carcinoma, Hepatocellular - drug therapy
Cell cycle
Cell Cycle Checkpoints - drug effects
Cell death
Cell Line, Tumor
Chemical compounds
Cytotoxicity
Hepatocellular carcinoma
Humans
Liver cancer
Liver Neoplasms - drug therapy
Mortality
Organelles
Phagocytosis
Pharmacology
Tumor cell lines
Usnic acid
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Summary:Usnic acid (UA) is a multifunctional bioactive lichen secondary metabolite with potential anti-cancer properties. Although the promising therapeutic effects of UA have been investigated in different cancer cell lines, the mechanism driving UA-induced cell death has yet to be elucidated. As the type of cell death (apoptosis or autophagy) induced by UA may vary depending on the cancer cell type, we first studied the cytotoxic effects of UA in HEPG2 (HBV(−)) and SNU-449(HBV(+)) hepatocellular carcinoma (HCC) cell lines. HCC cell viability was considerably reduced in a dose-dependent manner at 12, 24, and 48 h after treatment with UA (p < 0.05). However, SNU-449 cells were more sensitive to UA than HEPG2 cells. UA also induced apoptotic cell death in HCC cells with cell cycle arrest at G0/G1 and G2/M phase depending on the genetic profile of each cell type. On the other hand, we observed acidic vesicular organelles in HCC cells after 36 h of UA treatment. Taken together, these findings suggest that UA stimulates apoptosis and autophagy in HEPG2 and SNU-449 cells without damaging normal control cells. Thus, UA might be a potential therapeutic compound for HCC treatment. However, there is a need for further studies investigating the death-promoting or preventing roles for autophagy and the molecular signaling mechanisms induced by UA treatment.
ISSN:0960-3271
1477-0903
DOI:10.1177/0960327118792052