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• W2526915339 endingPage "7529" @default.
• W2526915339 startingPage "7520" @default.
• W2526915339 abstract "Ginsenoside Rh2 is a potential active metabolite of ginseng that has antitumor activity against a variety of tumor cells. Previously, we reported that Rh2-O, an octyl ester derivative of ginsenoside Rh2, had a higher anticancer activity than Rh2 through activating the intrinsic apoptotic pathway. In this study, we found that the extrinsic apoptotic pathway was also involved in Rh2-O-induced HepG2 cells apoptosis as evidenced by the up-regulation of Fas, FasL, TNFR1, and TNF-α as well as the cleavage of caspase 8. Moreover, flow cytometric analysis demonstrated that Rh2-O induced G1 cell cycle arrest in HepG2 cells. Rh2-O-induced G1 phase arrest was accompanied by the down-regulation of cyclin D3 and cyclin E and cyclin-dependent kinases (CDK) 4 and 6 and the up-regulation of p21WAF1/CIP1 and p27KIP1. In addition, Rh2-O down-regulated the phosphorylation of Akt, and its inhibitor LY294002 promoted Rh2-O-induced G1 phase arrest. Rh2-O treatment also activated p38 MAPK, JNK, and ERK expression. Inhibitors of p38 MAPK (SB203580), but not those of JNK (SP600125) or ERK (PB98095), promoted Rh2-O-induced G1 phase arrest in HepG2 cells. These results indicated that the disruption of Akt and p38 MAPK cascades played a pivotal role in Rh2-O-induced G1 phase arrest." @default.
• W2526915339 created "2016-10-07" @default.
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• W2526915339 date "2016-10-03" @default.
• W2526915339 modified "2023-09-23" @default.
• W2526915339 title "Octyl Ester of Ginsenoside Rh2 Induces Apoptosis and G1 Cell Cycle Arrest in Human HepG2 Cells by Activating the Extrinsic Apoptotic Pathway and Modulating the Akt/p38 MAPK Signaling Pathway" @default.
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• W2526915339 doi "https://doi.org/10.1021/acs.jafc.6b03519" @default.
• W2526915339 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27671480" @default.
• W2526915339 hasPublicationYear "2016" @default.
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