phorbol and phorbol-12-13-dibenzoate

phorbol has been researched along with phorbol-12-13-dibenzoate* in 3 studies

Other Studies

3 other study(ies) available for phorbol and phorbol-12-13-dibenzoate

ArticleYear
Phorbol esters inhibit the proliferation of MCF-7 cells. Possible implication of protein kinase C.
    Biochemical pharmacology, 1986, Aug-15, Volume: 35, Issue:16

    The effect of tumor promoter phorbol esters on cell proliferation was investigated in human breast cancer cell line MCF-7. During a 4-day culture period, the various phorbol ester derivatives TPA, PDD, PDBu, PDBz and PDA inhibited the proliferation of MCF-7 cells in a dose-dependent manner, with respective IC50 of 0.06, 0.75, 2.4, 3.6 and 15 X 10(-9) M. The 4-O-met-TPA, alpha PDD and alph PHR were ineffective at 2 X 10(-7) M, the highest concentration tested. Using a 3H-PDBu probe, we demonstrated the presence of specific, high affinity binding sites in intact cultured cells, with a Kd of about 9 X 10(-9) M. Unlabelled TPA, PDD, PDBU and PDBz competed with 3H-PDBu with respective IC50 of 35, 12.5, 150 and 220 X 10(-9) M. High concentrations of PDA, 4-O-met-TPA and alpha PDD slightly inhibited the 3H PDBu binding, whereas alpha PHR did not until 10(-5) M. The correlation that we observed between the relative potencies of the various phorbol derivatives for inhibiting both PDBu binding and cell proliferation, suggests that tumor promoter phorbol esters may induce growth arrest in MCF-7 cells by the mediation of protein kinase C.

    Topics: Breast Neoplasms; Cell Division; Cell Line; Dose-Response Relationship, Drug; Female; Humans; Phorbol 12,13-Dibutyrate; Phorbol Esters; Phorbols; Protein Kinase C; Tetradecanoylphorbol Acetate

1986
Co-mitogenic tumor promoters suppress the phosphatidylinositol response in lymphocytes during early mitogenesis.
    Biochimica et biophysica acta, 1985, Feb-08, Volume: 833, Issue:2

    The tumor-promoting agents 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and phorbol-12,13-dibenzoate inhibited the increased accumulation of [32P]phosphatidylinositol (PI) induced in mouse spleen lymphocytes by mitogenic lectins in the presence of [32P]orthophosphate. Similar inhibition of [32P]PI levels by TPA was seen in human tonsil T-lymphocytes stimulated with phytohemagglutinin. Only co-mitogenic phorbol esters prevented the [32P]PI accumulation during early mitogenesis. No increased 32P-labelling due to mitogen or decreases due to TPA was observed when cells were equilibrated with [32P]orthophosphate for 24 h prior to stimulation with mitogen, from which it is concluded that the total concentrations of phosphatidylcholine (PC) and PI are unaffected by mitogen or co-mitogen. The [32P]PI elevation but not the [32P]PC elevation was proportional to T-cell mitogenic potency for the lectins concanavalin A, divalent succinyl concanavalin A and phytohemagglutinin, and was prevented in each case by 5 X 10(-8) M TPA. Escherichia coli lipopolysaccharide did not give increased 32P incorporation into PI or PC, and TPA had no effect on 32P labelled phospholipid levels in the presence of this B-cell mitogen. The results indicate that the phosphatidylinositol response is not an invariable correlate of T-cell mitogenesis by polyclonal mitogens.

    Topics: Animals; Carcinogens; Female; Humans; Lymphocyte Activation; Mice; Phorbol Esters; Phorbols; Phosphates; Phosphatidylcholines; Phosphatidylinositols; Phytohemagglutinins; T-Lymphocytes; Tetradecanoylphorbol Acetate; Thymidine

1985
Effects of tumor-promoting agents on cells of the murine immune system: inhibition of antibody synthesis and of macrophage-mediated tumor cell cytotoxicity.
    Carcinogenesis; a comprehensive survey, 1982, Volume: 7

    Topics: Animals; Antibody Formation; B-Lymphocytes; Cytotoxicity, Immunologic; Female; Macrophages; Mice; Neoplasms, Experimental; Phorbol Esters; Phorbols; Structure-Activity Relationship; Tetradecanoylphorbol Acetate

1982