Antitumor Effect of Zinc Acetate in Hepatocellular Carcinoma Cell Lines via the Induction of Apoptosis

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  • HASHIMOTO Rie
    Department of Clinical Nutrition and Dietetics, Konan Women’s University Department of Gastroenterology and Neurology, Kagawa University School of Medicine
  • HIMOTO Takashi
    Department of Medical Technology, Kagawa Prefectural University of Health Sciences
  • YAMADA Mari
    Department of Gastroenterology and Neurology, Kagawa University School of Medicine
  • MIMURA Shima
    Department of Gastroenterology and Neurology, Kagawa University School of Medicine
  • FUJITA Koji
    Department of Gastroenterology and Neurology, Kagawa University School of Medicine
  • TANI Joji
    Department of Gastroenterology and Neurology, Kagawa University School of Medicine
  • MORISHITA Asahiro
    Department of Gastroenterology and Neurology, Kagawa University School of Medicine
  • MASAKI Tsutomu
    Department of Gastroenterology and Neurology, Kagawa University School of Medicine

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<p>We aimed to verify antitumor effects of zinc acetate on hepatocellular carcinoma (HCC) in vitro. Five HCC cell lines (HepG2, Hep3B, Huh7, HLE and Alex) were used to evaluate the antitumor effects of zinc acetate. Cell viability was determined by the Cell Counting Kit-8 assay. The cell-cycle alteration was evaluated by a flow cytometric analysis and the detection of cell cycle-related proteins. Apoptosis was determined based on the caspase-cleaved cytokeratin 18 (cCK18) levels. The microRNAs (miRNAs) related to an antitumor effect of zinc acetate were identified using microarrays. Zinc acetate significantly inhibited the proliferation of HCC cells in a dose-dependent manner. The treatment with zinc acetate resulted in significantly increased cCK18 levels in the supernatant and enhanced the expression of heme oxygenase-1 (HO-1) in HCC cells. The flow cytometric analysis revealed an increase of HCC cells in the S and G2/M phases by the administration of zinc acetate, and the expressions of Cdk2 and cyclin E were increased. The miRNA expression profile of the HCC cells treated with zinc acetate was extremely different from that of the untreated HCC cells. These results suggest that the zinc acetate supplementation induces the apoptosis of HCC cells, but does not affect the cell cycle progression. Upregulation of HO-1 and the alteration of miRNAs’ profile may be involved in antitumor effects of zinc acetate in HCC cells.</p>

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