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      Cell Death Induced by Baicalein in Human Hepatocellular Carcinoma Cell Lines

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          Abstract

          We examined the action of baicalein, a flavonoid contained in the herbal medicine sho‐saiko‐to (TJ‐9), on three cell lines of human hepatocellular carcinoma (HCC). Treatment with baicalein strongly inhibited the activity of topoisomerase II and suppressed the proliferation of all three HCC cell lines. But the mode of cell death induced by baicalein differed according to the cell line. Baicalein induced apoptosis in a concentration‐dependent mannner in only one cell line, and an increased concentration of baicalein produced cell death via necrosis in the other two lines. These results suggest that the inhibition of topoisomerase II is not by itself sufficient for induction of apoptosis, and that there is a more important mechanism which can account for the difference in susceptibility of cells to apoptosis induced by baicalein.

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          p53 is required for radiation-induced apoptosis in mouse thymocytes.

          S W Lowe, E Schmitt, S W Smith … (1993)
          The p53 tumour suppressor gene is the most widely mutated gene in human tumorigenesis. p53 encodes a transcriptional activator whose targets may include genes that regulate genomic stability, the cellular response to DNA damage, and cell-cycle progression. Introduction of wild-type p53 into cell lines that have lost endogenous p53 function can cause growth arrest or induce a process of cell death known as apoptosis. During normal development, self-reactive thymocytes undergo negative selection by apoptosis, which can also be induced in immature thymocytes by other stimuli, including exposure to glucocorticoids and ionizing radiation. Although normal negative selection involves signalling through the T-cell receptor, the induction of apoptosis by other stimuli is poorly understood. We have investigated the requirement for p53 during apoptosis in mouse thymocytes. We report here that immature thymocytes lacking p53 die normally when exposed to compounds that may mimic T-cell receptor engagement and to glucocorticoids but are resistant to the lethal effects of ionizing radiation. These results demonstrate that p53 is required for radiation-induced cell death in the thymus but is not necessary for all forms of apoptosis.
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            Thymocyte apoptosis induced by p53-dependent and independent pathways.

            A R Clarke, C A Purdie, D Harrison … (1993)
            Death by apoptosis is characteristic of cells undergoing deletion during embryonic development, T- and B-cell maturation and endocrine-induced atrophy. Apoptosis can be initiated by various agents and may be a result of expression of the oncosuppressor gene p53 (refs 6-8). Here we study the dependence of apoptosis on p53 expression in cells from the thymus cortex. Short-term thymocyte cultures were prepared from mice constitutively heterozygous or homozygous for a deletion in the p53 gene introduced into the germ line after gene targeting. Wild-type thymocytes readily undergo apoptosis after treatment with ionizing radiation, the glucocorticoid methylprednisolone, or etoposide (an inhibitor of topoisomerase II), or after Ca(2+)-dependent activation by phorbol ester and a calcium ionophore. In contrast, homozygous null p53 thymocytes are resistant to induction of apoptosis by radiation or etoposide, but retain normal sensitivity to glucocorticoid and calcium. The time-dependent apoptosis that occurs in untreated cultures is unaffected by p53 status. Cells heterozygous for p53 deletion are partially resistant to radiation and etoposide. Our results show that p53 exerts a significant and dose-dependent effect in the initiation of apoptosis, but only when it is induced by agents that cause DNA-strand breakage.
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              A simple, rapid, and sensitive DNA assay procedure.

              Cesar Labarca, Kenneth Paigen (1980)
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                Author and article information

                Journal
                Journal ID (nlm-ta): Jpn J Cancer Res
                Journal ID (iso-abbrev): Jpn. J. Cancer Res
                Journal ID (doi): 10.1111/(ISSN)1349-7006a
                Journal ID (publisher-id): CAS
                Title: Japanese Journal of Cancer Research : Gann
                Publisher: Blackwell Publishing Ltd (Oxford, UK )
                ISSN (Print): 0910-5050
                ISSN (Electronic): 1876-4673
                Publication date (Print): February 1996
                Volume: 87
                Issue: 2 ( doiID: 10.1111/cas.1996.87.issue-2 )
                Pages: 170-177
                Affiliations
                [ 1 ]First Department of Internal Medicine, Yamaguchi University School of Medicine, 1144 Kogushi, Ube, Yatnaguchi 755
                [ 2 ]Department of Virology and Parasitology, Yamaguchi University School of Medicine, 1144 Kogushi, Ube, Yatnaguchi 755
                Author notes
                [*] [* ]To whom correspondence should be addressed.
                Article
                Publisher ID: CAE170
                DOI: 10.1111/j.1349-7006.1996.tb03155.x
                PMC ID: 5921056
                PubMed ID: 8609066
                SO-VID: 3b95cd63-e572-4ab6-90d7-a880b7724ab9
                History
                Page count
                References: 47, Pages: 8
                Categories
                Subject: Article
                Custom metadata
                source-schema-version-number 2.0
                cover-date February 1996
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:4.6.9 mode:remove_FC converted:04.11.2015

                Keywords: baicalein,apoptosis,hepatocellular carcinoma,sho‐saiko‐to (tj‐9),cell death
                Data availability:
                Keywords: baicalein, apoptosis, hepatocellular carcinoma, sho‐saiko‐to (tj‐9), cell death

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