moxestrol has been researched along with Liver-Neoplasms* in 2 studies
2 other study(ies) available for moxestrol and Liver-Neoplasms
| Article | Year |
|---|---|
Regulation of sex hormone-binding globulin secretion in human hepatoma G2 cells.
Our purpose was to examine the roles of natural (estradiol (E2) and estrone (E1)) and synthetic estrogens (ethinyl estradiol (EE), moxestrol (MOX), and tamoxifene (TAM)) in regulating production of sex hormone-binding globulin (SHBG) by human hepatoma G2 (Hep G2) cells, the rationale being that synthetic estrogens are less rapidly metabolized than natural estrogens and, thus, may alter SHBG levels more readily. In Hep G2 cells, E2, E1, and EE at 10(-7) M did not result in significantly greater SHBG secretion compared to control cells. The synthetic estrogens, MOX and TAM, caused significant, P < 0.001, increases of 30% and 51% in SHBG secretion at 10(-7) M compared to controls. However, when TAM and E2 were added together, each at 10(-7) M, no increase in SHBG secretion was noted. We conclude that natural estrogens at physiologic concentrations do not increase SHBG secretion by Hep G2 cells, but the increase of SHBG secretion caused by MOX and TAM suggests that the lack of effect of E2 and E1 may, in part, be due to their rapid metabolism. In addition, TAM stimulates SHBG secretion by interaction with the genome that is different, in certain respects, from that of E2. Topics: Antineoplastic Agents, Hormonal; Carcinoma, Hepatocellular; Dose-Response Relationship, Drug; Estradiol; Estradiol Congeners; Estrone; Ethinyl Estradiol; Humans; Liver Neoplasms; Sex Hormone-Binding Globulin; Tamoxifen; Time Factors; Tumor Cells, Cultured | 2001 |
Characterization of the "estrogenicity" of tamoxifen and raloxifene in HepG2 cells: regulation of gene expression from an ERE controlled reporter vector versus regulation of the endogenous SHBG and PS2 genes.
The estrogenic character of tamoxifen and raloxifene was studied on three different genes, an ERE-reporter construct and two endogenous genes, sex hormone binding globulin (SHBG) and pS2, in two variants of the human liver carcinoma cell line HepG2. On the ERE-reporter construct and the pS2 gene both tamoxifen and raloxifene acted as pure estrogen antagonists, whereas on the SHBG gene they functioned as partial estrogens/antiestrogens at concentrations below 1 microM and as full "agonists" at concentrations higher than 1 microM. The fold stimulatory effect of tamoxifen and raloxifene on SHBG protein expression was similar in the estrogen receptor (ER) expressing HepG2 cells (HepER3) and the parental non-ER expressing HepG2 cells at concentrations above 1 microM. In contrast, the 17beta-estradiol analogue moxestrol stimulated SHBG expression only in the HepER3 cells. Both tamoxifen and raloxifene had an additive effect to estrogen receptor-dependent SHBG gene expression in the HepER3 cells in the presence of saturating concentrations of moxestrol. However, a significant difference was observed in that a much higher concentration of moxestrol was required to see an additive effect of raloxifene compared to tamoxifen. The cytokine IL1-beta completely blocked the tamoxifen-dependent induction of SHBG gene expression in HepER3 cells, but only partly blocked the effect of moxestrol mediated by the ER. In conclusion, our results suggest that the mechanism for the liver-selective "estrogenic" character of tamoxifen and raloxifene is mediated by a non-ER dependent pathway. Topics: Alkaline Phosphatase; Carcinoma, Hepatocellular; Clone Cells; Estradiol; Estradiol Congeners; Estrogen Antagonists; Ethinyl Estradiol; Female; Gene Expression Regulation, Neoplastic; Genes, Reporter; Humans; Kinetics; Liver Neoplasms; Piperidines; Placenta; Pregnancy; Protein Biosynthesis; Proteins; Raloxifene Hydrochloride; Receptors, Estrogen; Recombinant Fusion Proteins; Sex Hormone-Binding Globulin; Tamoxifen; Tetradecanoylphorbol Acetate; Trefoil Factor-1; Tumor Cells, Cultured; Tumor Suppressor Proteins | 1997 |