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  4. 4-acetylantroquinonol B isolated from antrodia cinnamomea arrests proliferation of human hepatocellular carcinoma HepG2 cell by affecting p53, p21 and p27 levels
 
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4-acetylantroquinonol B isolated from antrodia cinnamomea arrests proliferation of human hepatocellular carcinoma HepG2 cell by affecting p53, p21 and p27 levels

Journal
Journal of Agricultural and Food Chemistry
Journal Volume
59
Journal Issue
16
Pages
8625-8631
Date Issued
2011
Author(s)
Lin Y.-W.
Chiang B.-H.  
DOI
10.1021/jf2011326
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/413298
URL
https://www.scopus.com/inward/record.uri?eid=2-s2.0-80051727402&doi=10.1021%2fjf2011326&partnerID=40&md5=dcf4c28de3006f69c3614ddfc2062bc4
Abstract
The 4-acetylantroquinonol B isolated from the mycelium of Antrodia cinnamomea could inhibit proliferation of hepatocellular carcinoma cells HepG2 with IC 50 0.1 £gg/mL. When the HepG2 cells were treated with 4-acetylantroquinonol B for 72 h, the proportion of cells in the G1 phase of the cell cycle increased and that in the S phase decreased significantly, and the proportion of G2/M phase cells were not obviously changed. In addition, the 4-acetylantroquinonol B treatment resulted in the decreases of CDK2 and CDK4, and an increase of p27 in a dose-dependent manner. The protein levels of p53 and p21 proteins were also increased when the cells were treated with low dosage (0.1 £gg/mL) of 4-acetylantroquinonol B. Higher dosages, however, decreased the expression of p53 and p21 proteins. Assay of RT-PCR indicated that, corresponding to the increases of p53 and p21 proteins at the dosage of 0.1 £gg/mL, the mRNAs of p53 and p21 showed 1.66- and 1.61-fold upregulations, respectively. Corresponding to the decreases of CDK2 and CDK4 proteins, the mRNAs of CDK2 and CDK4 showed -1.02- and -1.13-fold downregulations, respectively. However, level of p27 mRNA showed -1.2-fold downregulation in spite of the increase in p27 protein. This observation, again, confirms the fact that the p27 gene rarely undergoes homozygous inactivation in cancer cells. Our finding suggested that the 4-acetylantroquinonol B inhibits proliferation of HepG2 cells via affecting p53, p21 and p27 proteins, and can be considered as a potential cancer drug. ? 2011 American Chemical Society.
Subjects
4-acetylantroquinonol B
Antrodia cinnamomea
cell cycle regulators
hepatocellular carcinoma cells
HepG2
p27 protein
SDGs

[SDGs]SDG3

Other Subjects
4-acetylantroquinonol B; Antrodia cinnamomea; Cell cycle regulators; Hepatocellular carcinoma cell; HepG2; p27 protein; Cells; Diseases; Genes; Proteins; Cytology; 4 acetylantroquinonol B; 4-acetylantroquinonol B; antineoplastic agent; CDKN1A protein, human; cyclin dependent kinase inhibitor 1A; cyclin dependent kinase inhibitor 1B; cyclohexanone derivative; drug derivative; gamma butyrolactone; protein p53; Antrodia; article; cell cycle G1 phase; cell cycle S phase; cell proliferation; cell strain HepG2; chemistry; drug effect; human; isolation and purification; 4-Butyrolactone; Antineoplastic Agents; Antrodia; Cell Proliferation; Cyclin-Dependent Kinase Inhibitor p21; Cyclin-Dependent Kinase Inhibitor p27; Cyclohexanones; G1 Phase; Hep G2 Cells; Humans; S Phase; Tumor Suppressor Protein p53; Antrodia cinnamomea
Type
journal article

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