|Oridonin induces G2/M cell cycle arrest and apoptosis through MAPK and p53 signaling pathways in HepG2 cells.|
|PMID: 20664969 Owner: NLM Status: MEDLINE|
|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. IC50 values were determined as 38.86 microM and 24.90 microM for 24-h and 48-h treatments, respectively. Flow cytometric analysis showed that a 24-h treatment of 40 microM 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.|
|Hui Wang; Yan Ye; Jian-Hong Chui; Guo-Yuan Zhu; Ying-Wei Li; David W F Fong; Zhi-Ling Yu|
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|Type: Journal Article; Research Support, Non-U.S. Gov't|
|Title: Oncology reports Volume: 24 ISSN: 1791-2431 ISO Abbreviation: Oncol. Rep. Publication Date: 2010 Sep|
|Created Date: 2010-07-28 Completed Date: 2010-11-23 Revised Date: -|
Medline Journal Info:
|Nlm Unique ID: 9422756 Medline TA: Oncol Rep Country: Greece|
|Languages: eng Pagination: 647-51 Citation Subset: IM|
|Center for Cancer and Inflammation Research, School of Chinese Medicine, Hong Kong Baptist University, Kowloon Tong, Hong Kong, PR China.|
|APA/MLA Format Download EndNote Download BibTex|
Antineoplastic Agents, Phytogenic
Apoptosis / drug effects*
Carcinoma, Hepatocellular / enzymology, pathology*
Caspase 3 / metabolism
Caspase 9 / metabolism
Cell Cycle / drug effects*
Cell Survival / drug effects
Cyclin B / metabolism
Cyclin B1 / metabolism
Cyclin-Dependent Kinase Inhibitor p21 / metabolism
Diterpenes, Kaurane / pharmacology*
Dose-Response Relationship, Drug
Extracellular Signal-Regulated MAP Kinases / metabolism
Hep G2 Cells
Inhibitory Concentration 50
JNK Mitogen-Activated Protein Kinases / metabolism
Liver Neoplasms / enzymology, pathology*
MAP Kinase Signaling System / drug effects*
Tumor Suppressor Protein p53 / metabolism*
p38 Mitogen-Activated Protein Kinases / metabolism
|0/Antineoplastic Agents, Phytogenic; 0/CCNB1 protein, human; 0/CDC2 protein, human; 0/CDKN1A protein, human; 0/Cyclin B; 0/Cyclin B1; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Diterpenes, Kaurane; 0/TP53 protein, human; 0/Tumor Suppressor Protein p53; 28957-04-2/oridonin; EC 188.8.131.52/Extracellular Signal-Regulated MAP Kinases; EC 184.108.40.206/JNK Mitogen-Activated Protein Kinases; EC 220.127.116.11/p38 Mitogen-Activated Protein Kinases; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/CASP9 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 9|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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