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Sinularin induces DNA damage, G2/M phase arrest, and apoptosis in human hepatocellular carcinoma cells
Ting-Wen Chung1, Shih-Chao Lin2,3, Jui-Hsin Su4
1Institute of Bioinformatics and Structural Biology and Department of Medical Sciences, National Tsing Hua University, Hsinchu, Taiwan.
Background:
Sinularin isolated from the cultured soft coral Sinularia flexibilis has been reported to exert potent cytotoxic effects against particular types of cancer. This study was carried out to investigate the cytotoxic effects in sinularin-treated human hepatocellular carcinoma cells, HepG2, and to subsequently explore the underlying molecular mechanisms.
Methods:
TheMTT (3-[4,5-dimethylthiazol-2-yl]-2, 5-diphenyl- tetrazolium bromide) method was used to evaluate the cytotoxicity of sinularin on HepG2 and Hep3B cell lines. Furthermore, the cell cycle distribution assay, apoptosis assay, and western blot analysis in vitro were used to explore the possible mechanisms of action.
Results:
From the results of our study, cell viability was obviously inhibited by sinularin in a dose-dependent manner. In addition, our results suggested that sinularin triggered DNA damage and subsequently induced cell cycle G2/M arrest associated with up-regulation of p-ATM (Ser(1981)), p-Chk2 (Tyr(68)), p-cdc2 (Tyr(15)), and p53 coupled with increased expression of downstream proteins p21 and down-regulation of p-cdc25 (Ser(216)). Moreover, the results of the apoptosis assay and western blot analysis indicated that the cytotoxic activity could be related to mitochondrial apoptosis, characterized by decrease of Bcl-2 expression, disruption of mitochondrial membrane potential, and sequential activation of caspases and Poly (ADP-ribose) polymerase (PARP).
Conclusions:
This study reveals for the first time the anti-HCC activities of sinularin, the active compound isolated from the cultured soft coral Sinularia flexibilis. We believe that our results warrant further evaluation of sinularin as a new anti-HCC chemotherapeutic agent.
Insights
Sinularin from soft coral inhibits hepatocellular carcinoma (HCC) cell viability by inducing DNA damage and mitochondrial apoptosis. Further research is warranted for its potential as an anti-HCC chemotherapeutic agent.
Area of Science:
- Marine natural products chemistry
- Cancer biology
- Molecular pharmacology
Background:
- Sinularin, a compound from soft coral Sinularia flexibilis, exhibits cytotoxic effects against certain cancers.
- Hepatocellular carcinoma (HCC) remains a significant global health challenge.
Purpose of the Study:
- To investigate the cytotoxic effects of sinularin on human hepatocellular carcinoma (HCC) cells (HepG2).
- To elucidate the molecular mechanisms underlying sinularin's anti-cancer activity.
Main Methods:
- Cytotoxicity was assessed using the MTT assay on HepG2 and Hep3B cell lines.
- Mechanisms were explored via cell cycle distribution, apoptosis assays, and western blot analysis.
Main Results:
- Sinularin demonstrated dose-dependent inhibition of HepG2 cell viability.
- It induced DNA damage, G2/M cell cycle arrest, and mitochondrial apoptosis.
- Key molecular changes included altered expression of ATM, Chk2, p53, p21, Bcl-2, and activation of caspases and PARP.
Conclusions:
- Sinularin exhibits significant anti-HCC activities.
- The compound induces apoptosis through the mitochondrial pathway.
- Sinularin shows promise as a potential chemotherapeutic agent for HCC.
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