Abstract
Liriodenine was isolated from the leaves of Michelia compressa. This study was designed to assess cell cycle arrest, the production of nitric oxide (NO) and p53 expression in liriodenine-treated human hepatoma cell lines, including wild-type p53 (Hep G2 and SK-Hep-1). As evidenced by flowcytometric studies, liriodenine induced cell cycle G(1) arrest and inhibited DNA synthesis in Hep G2 and SK-Hep-1 cell lines. The p53, iNOS expression and intracellular NO level were markedly increased in Hep G2 cells after liriodenine treatment. A NO inhibitor, carboxy-PTIO inhibited the p53 expression induced by liriodenine. In addition, liriodenine could not induce obvious cytotoxicity in normal human IMR-90 cell line. These results demonstrate that NO production and p53 expression are critical factors in liriodenine-induced growth inhibition in human wild-type p53 hepatoma cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antimetabolites
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Antineoplastic Agents, Phytogenic / chemistry
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Antineoplastic Agents, Phytogenic / pharmacology*
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Aporphines / chemistry
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Aporphines / pharmacology*
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Blotting, Western
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Bromodeoxyuridine
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Carcinoma, Hepatocellular / pathology*
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Cell Cycle / drug effects*
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Cell Proliferation / drug effects*
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Chromatography, Thin Layer
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DNA, Neoplasm / biosynthesis
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Dose-Response Relationship, Drug
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Flow Cytometry
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Gene Expression / drug effects
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Genes, p53 / drug effects*
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Humans
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Magnetic Resonance Spectroscopy
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Magnoliaceae / chemistry
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Nitric Oxide / physiology*
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Nitric Oxide Synthase / biosynthesis
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Nitric Oxide Synthase Type II
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Spectrophotometry, Infrared
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Spectrophotometry, Ultraviolet
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Tumor Cells, Cultured
Substances
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Antimetabolites
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Antineoplastic Agents, Phytogenic
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Aporphines
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DNA, Neoplasm
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Nitric Oxide
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liriodenine
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NOS2 protein, human
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Nitric Oxide Synthase
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Nitric Oxide Synthase Type II
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Bromodeoxyuridine