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Inhibition by dexamethasone of transforming growth factor beta1-induced apoptosis in rat hepatoma cells: a possible association with Bcl-xL induction.

Abstract

The authors previously reported that transforming growth factor beta1 (TGF-beta1) induces apoptosis in McA-RH7777 (7777) and McA-RH8994 (8994) rat hepatoma cell lines. Although these cell lines exhibit different responses to glucocorticoid treatment in various cellular functions and gene expression, dexamethasone (DEX) inhibited spontaneous and TGF-beta1-induced apoptosis in both. Analysis of analogous hormones in TGF-beta1-induced apoptosis in 8994 cells suggested the inhibitory effect to be glucocorticoid-specific. By cell-cycle analysis and DNA fragmentation assay using sodium butyrate, a G1-arrest-inducing reagent, regulation of apoptosis by TGF-beta1 and DEX was shown independent of the cell cycle. For elucidation of the mechanisms of anti-apoptotic action of DEX, the effects of various chemical probes on this apoptosis model were examined, and various reagents known to exhibit anti-apoptotic activity in other experimental systems were found to be ineffective. The effect of TGF-beta1 and DEX on cellular amounts of several apoptosis-related proteins, members of the Bcl-2 family, Bcl-2, Bcl-xL, Bcl-xS, Bad, and Bax was also examined. DEX drastically increased Bcl-xL in both cell lines irrespective of the presence of TGF-beta1. Bcl-2 and Bcl-xS proteins were not detected, and Bax and Bad content did not change by treatment with TGF-beta1 or DEX. Progesterone (Prog), a partial antagonist for glucocorticoid receptor, inhibited the effects of DEX on apoptosis and Bcl-xL expression in 8994 cells. Thus, Bcl-xL induction by DEX would appear closely associated with its inhibitory effect on spontaneous and TGF-beta1-induced apoptosis in the hepatoma cell lines.

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  • Authors+Show Affiliations

    ,

    Kampo Pharmacology Department, Tsumura and Co., Ami, Ibaraki, Japan.

    , , , ,

    Source

    Hepatology (Baltimore, Md.) 27:4 1998 Apr pg 959-66

    MeSH

    Animals
    Apoptosis
    Cell Cycle
    Cell Division
    Dexamethasone
    Liver Neoplasms, Experimental
    Proto-Oncogene Proteins c-bcl-2
    Rats
    Transforming Growth Factor beta
    Tumor Cells, Cultured
    bcl-X Protein

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    9537434

    Citation

    Yamamoto, M, et al. "Inhibition By Dexamethasone of Transforming Growth Factor Beta1-induced Apoptosis in Rat Hepatoma Cells: a Possible Association With Bcl-xL Induction." Hepatology (Baltimore, Md.), vol. 27, no. 4, 1998, pp. 959-66.
    Yamamoto M, Fukuda K, Miura N, et al. Inhibition by dexamethasone of transforming growth factor beta1-induced apoptosis in rat hepatoma cells: a possible association with Bcl-xL induction. Hepatology. 1998;27(4):959-66.
    Yamamoto, M., Fukuda, K., Miura, N., Suzuki, R., Kido, T., & Komatsu, Y. (1998). Inhibition by dexamethasone of transforming growth factor beta1-induced apoptosis in rat hepatoma cells: a possible association with Bcl-xL induction. Hepatology (Baltimore, Md.), 27(4), pp. 959-66.
    Yamamoto M, et al. Inhibition By Dexamethasone of Transforming Growth Factor Beta1-induced Apoptosis in Rat Hepatoma Cells: a Possible Association With Bcl-xL Induction. Hepatology. 1998;27(4):959-66. PubMed PMID: 9537434.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Inhibition by dexamethasone of transforming growth factor beta1-induced apoptosis in rat hepatoma cells: a possible association with Bcl-xL induction. AU - Yamamoto,M, AU - Fukuda,K, AU - Miura,N, AU - Suzuki,R, AU - Kido,T, AU - Komatsu,Y, PY - 1998/4/16/pubmed PY - 1998/4/16/medline PY - 1998/4/16/entrez SP - 959 EP - 66 JF - Hepatology (Baltimore, Md.) JO - Hepatology VL - 27 IS - 4 N2 - The authors previously reported that transforming growth factor beta1 (TGF-beta1) induces apoptosis in McA-RH7777 (7777) and McA-RH8994 (8994) rat hepatoma cell lines. Although these cell lines exhibit different responses to glucocorticoid treatment in various cellular functions and gene expression, dexamethasone (DEX) inhibited spontaneous and TGF-beta1-induced apoptosis in both. Analysis of analogous hormones in TGF-beta1-induced apoptosis in 8994 cells suggested the inhibitory effect to be glucocorticoid-specific. By cell-cycle analysis and DNA fragmentation assay using sodium butyrate, a G1-arrest-inducing reagent, regulation of apoptosis by TGF-beta1 and DEX was shown independent of the cell cycle. For elucidation of the mechanisms of anti-apoptotic action of DEX, the effects of various chemical probes on this apoptosis model were examined, and various reagents known to exhibit anti-apoptotic activity in other experimental systems were found to be ineffective. The effect of TGF-beta1 and DEX on cellular amounts of several apoptosis-related proteins, members of the Bcl-2 family, Bcl-2, Bcl-xL, Bcl-xS, Bad, and Bax was also examined. DEX drastically increased Bcl-xL in both cell lines irrespective of the presence of TGF-beta1. Bcl-2 and Bcl-xS proteins were not detected, and Bax and Bad content did not change by treatment with TGF-beta1 or DEX. Progesterone (Prog), a partial antagonist for glucocorticoid receptor, inhibited the effects of DEX on apoptosis and Bcl-xL expression in 8994 cells. Thus, Bcl-xL induction by DEX would appear closely associated with its inhibitory effect on spontaneous and TGF-beta1-induced apoptosis in the hepatoma cell lines. SN - 0270-9139 UR - https://www.unboundmedicine.com/medline/citation/9537434/Inhibition_by_dexamethasone_of_transforming_growth_factor_beta1_induced_apoptosis_in_rat_hepatoma_cells:_a_possible_association_with_Bcl_xL_induction_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0270913998001438 DB - PRIME DP - Unbound Medicine ER -