Abstract |
The aim of the present study was to evaluate the antitumor mechanism of dihydromyricetin (DHM). Results showed that DHM significantly inhibited cell viability of HepG2 and Hep3B cells in a dose-dependent manner. DHM induced G2/M cell-cycle arrest in HepG2 and Hep3B cells by altering the expression of cell cycle proteins such as cyclin A, cyclin B1, Cdk1, p53, Cdc25c, p-Cdc25c Chk1 and Chk, which are critical for G2/M transition. Knockdown of p53 and Chk1 in HepG2 cells did not affect G2/M phase arrest caused by DHM. Furthermore, G2/M arrest induced by DHM can be disrupted by Chk2 siRNA. These findings indicate that DHM inhibits the growth of hepatocellular carcinoma (HCC) cells via G2/M phase cell cycle arrest through Chk1/Chk2/Cdc25C pathway. The present study identified effects of DHM in G2/M phase arrest in HCC and described detailed mechanisms of G2/M phase arrest by this agent, which may contribute to its overall cancer preventive efficacy in HCC.
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Authors | Haili Huang, Min Hu, Rui Zhao, Peng Li, Mingyi Li |
Journal | Oncology reports
(Oncol Rep)
Vol. 30
Issue 5
Pg. 2467-75
(Nov 2013)
ISSN: 1791-2431 [Electronic] Greece |
PMID | 24002546
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Flavonols
- Protein Kinases
- Checkpoint Kinase 2
- CHEK1 protein, human
- CHEK2 protein, human
- Checkpoint Kinase 1
- CDC25C protein, human
- cdc25 Phosphatases
- dihydromyricetin
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Topics |
- Carcinoma, Hepatocellular
(drug therapy, genetics, pathology)
- Cell Proliferation
(drug effects)
- Checkpoint Kinase 1
- Checkpoint Kinase 2
(biosynthesis, genetics)
- Flavonols
(pharmacology)
- G2 Phase Cell Cycle Checkpoints
(drug effects)
- Gene Expression Regulation, Neoplastic
(drug effects)
- Hep G2 Cells
- Humans
- Liver Neoplasms
(drug therapy, genetics, pathology)
- Protein Kinases
(biosynthesis, genetics)
- Signal Transduction
(drug effects)
- cdc25 Phosphatases
(biosynthesis, genetics)
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