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  • Title: Psoralidin inhibits the proliferation of human liver cancer cells by triggering cell cycle arrest, apoptosis and autophagy and inhibits tumor growth in vivo.
    Author: Li J, Fu Y, Hu X, Xiong Y.
    Journal: J BUON; 2019; 24(5):1950-1955. PubMed ID: 31786860.
    Abstract:
    PURPOSE: Liver cancer is a lethal malignancy with high mortality. Approximately 0.56 million new cases of liver cancer are reported annually. The adverse effects of currently available inefficient chemotherapy remarkably obstruct the treatment of liver cancer. This study was undertaken to investigate the anticancer effects of a natural coumarin, Psoralidin, in vitro and in vivo. METHODS: The liver HepG2 cancer cell line was used in this study. The MTT cell viability assay was used for the determination of the proliferation rate. Flow cytometry was used for cell cycle analysis. DAPI was used for detection of apoptosis and transmission electron microscopy (TEM) analysis was performed for the demonstration of autophagy. Protein expression was estimated by western blot analysis. RESULTS: Psoralidin decreased the viability of the liver cancer HepG2 cells and exhibited an IC50 of 9 µM. Also, Psoralidin exerted very low toxic effects on the normal AML12 hepatocytes exhibiting an IC50 of 100 µM. Flow cytometry showed that Psoralidin triggered G2/M cell cycle arrest of the HepG2 cancer cells. DAPI staining revealed that Psoralidin triggered apoptotic cell death of HepG2 cells which was accompanied with activation of caspases 3 and 9, upregulation of Bax and downregulation of Bcl-2. Additionally, Psoralidin prompted autophagy in the HepG2 cells as revealed by TEM. The Psoralidin-induced autophagy led to upregulation of LC3 II and Beclin-1 expression. Investigation of the in vivo anticancer potential of Psoralidin revealed that this molecule could suppress the growth of xenografted tumors in vivo. CONCLUSION: Psoralidin may prove essential in the development of systemic therapy for liver cancer.
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