http://dx.doi.org/10.3892/or_00000903">
 

Document Type

Journal Article

Department/Unit

School of Chinese Medicine

Title

Oridonin induces G2/M cell cycle arrest and apoptosis through MAPK and p53 signaling pathways in HepG2 cells

Language

English

Abstract

Oridonin, the main active constituent of Isodon rubescen, has antihepatocarcinoma activity in experimental and clinical settings. The aims of the study were to explore the anticancer effect of oridonin in HepG2 cells and to investigate the underlying mechanisms. Results showed that oridonin treatment for 24 or 48 h resulted in a marked decrease in cell viability time- and dose-dependently. IC 50 values were determined as 38.86 μM and 24.90 μM for 24-h and 48-h treatments, respectively. Flow cytometric analysis showed that a 24-h treatment of 40 μM oridonin induced G2/M cell cycle arrest and apoptosis. Typical apoptotic nucleus alterations were observed with fluorescence microscope after DAPI staining. Immunoblot analysis demonstrated that oridonin treatment increased expression levels of p-JNK, p-p38, p-p53 and p21, elevated the level of cyclin B1/p-Cdc2 (Tyr15) complex, and inhibited the expression of p-ERK. Moreover, oridonin treatment activated caspase-9 and caspase-3. In conclusion, oridonin induced G2/M cell cycle arrest and apoptosis in HepG2 cells through MAPK and p53 pathways, which advances our understanding on the molecular mechanisms of oridonin in hepatocarcinoma management.

Keywords

Apoptosis, G2/M arrest, HepG2, MAPK, Oridonin, p53

Publication Date

2010

Source Publication Title

Oncology Reports

Volume

24

Issue

3

Start Page

647

End Page

651

Publisher

Spandidos Publications

ISSN (print)

1021335X

ISSN (electronic)

17912431

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