Dihydromyricetin promotes hepatocellular carcinoma regression via a p53 activation-dependent mechanism

The development of antitumor chemotherapy drugs remains a key goal for oncologists and natural products provide a vast resource for anti-cancer drug discovery. In the current study, we found that the flavonoid dihydromyricetin (DHM) exhibited antitumor activity against liver cancer cells, including...

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Bibliographic Details
Published in:Scientific reports 2014-04, Vol.4 (1), p.4628-4628, Article 4628
Main Authors: Zhang, Qingyu, Liu, Jie, Liu, Bin, Xia, Juan, Chen, Nianping, Chen, Xiaofeng, Cao, Yi, Zhang, Chen, Lu, CaiJie, Li, Mingyi, Zhu, Runzhi
Format: Article
Language:English
Subjects:
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13/106
13/109
13/2
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13/51
13/89
13/95
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38
631/67/2195
692/420/755
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Animals
Antineoplastic Agents - pharmacology
Antineoplastic Combined Chemotherapy Protocols - pharmacology
Apoptosis - drug effects
Carcinoma, Hepatocellular - drug therapy
Cell Line, Tumor
Cell Proliferation - drug effects
Cisplatin - pharmacology
Drug discovery
Enzyme Activation - drug effects
Flavonols - pharmacology
Growth inhibition
Hep G2 Cells
Humanities and Social Sciences
Humans
Liver - cytology
Liver - pathology
Liver cancer
Liver Neoplasms - drug therapy
Male
Medicine, Chinese Traditional
Mice
Mice, Inbred BALB C
Mice, Nude
multidisciplinary
p53 Protein
Phosphorylation - drug effects
RNA Interference
RNA, Small Interfering
Science
Signal transduction
Signal Transduction - drug effects
Tumor Suppressor Protein p53 - biosynthesis
Tumor Suppressor Protein p53 - metabolism
Tumors
Xenograft Model Antitumor Assays
Xenografts
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Summary:The development of antitumor chemotherapy drugs remains a key goal for oncologists and natural products provide a vast resource for anti-cancer drug discovery. In the current study, we found that the flavonoid dihydromyricetin (DHM) exhibited antitumor activity against liver cancer cells, including primary cells obtained from hepatocellular carcinoma (HCC) patients. In contrast, DHM was not cytotoxic to immortalized normal liver cells. Furthermore, DHM treatment resulted in the growth inhibition and remission of xenotransplanted tumors in nude mice. Our results further demonstrated that this antitumor activity was caused by the activation of the p53-dependent apoptosis pathway via p53 phosphorylation at serine (15Ser). Moreover, our results showed that DHM plays a dual role in the induction of cell death when administered in combination with cisplatin, a common clinical drug that kills primary hepatoma cells but not normal liver cells.
ISSN:2045-2322
2045-2322
DOI:10.1038/srep04628