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

Hui Wang, Yan Ye, Jian Hong Chu, Guo Yuan Zhu, Ying Wei Li, David W F FONG, Zhiling YU*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

46 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)647-651
Number of pages5
JournalOncology Reports
Volume24
Issue number3
DOIs
Publication statusPublished - Sep 2010

Scopus Subject Areas

  • Oncology
  • Cancer Research

User-Defined Keywords

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

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