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Dihydromyricetin promotes hepatocellular carcinoma regression via a p53 activation-dependent mechanism
Qingyu Zhang1, Jie Liu1, Bin Liu1
1Key Laboratory of Hepatic Disease, Department of Hepatobiliary Surgery, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, China.
Abstract:
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.
Insights
The natural compound dihydromyricetin (DHM) shows potent antitumor effects against liver cancer cells and tumors. It selectively targets cancer cells by activating the p53 pathway, offering a promising avenue for novel liver cancer therapies.
Area of Science:
- Oncology
- Natural Product Chemistry
- Molecular Biology
Background:
- Natural products are a vital source for developing new anti-cancer drugs.
- Hepatocellular carcinoma (HCC) remains a significant global health challenge requiring novel therapeutic strategies.
Purpose of the Study:
- To investigate the potential antitumor activity of the flavonoid dihydromyricetin (DHM) against liver cancer.
- To elucidate the molecular mechanisms underlying DHM's anti-cancer effects.
Main Methods:
- In vitro assays using primary hepatocellular carcinoma (HCC) cells and immortalized normal liver cells.
- In vivo studies involving xenotransplanted tumors in nude mice.
- Western blot analysis to assess p53 phosphorylation and apoptosis pathway activation.
Main Results:
- Dihydromyricetin (DHM) demonstrated significant antitumor activity against HCC cells and xenograft tumors.
- DHM selectively inhibited the growth of cancer cells while sparing normal liver cells.
- The anti-cancer effect was attributed to the activation of p53-dependent apoptosis via p53 phosphorylation at serine 15 (15Ser).
- DHM exhibited a synergistic effect with cisplatin in inducing cancer cell death.
Conclusions:
- Dihydromyricetin (DHM) is a promising natural compound with selective antitumor activity against liver cancer.
- DHM's mechanism involves the p53 signaling pathway, making it a potential therapeutic agent.
- Combination therapy with DHM and cisplatin warrants further investigation for enhanced liver cancer treatment.
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