Androgens inhibit estrogen action in MCF-7 human breast cancer cells

MacIndoe, John H.; Etre, Lois A.

doi:10.1016/0024-3205(80)90637-2

Cited by 32 publications

(2 citation statements)

References 3 publications

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“…Finally, a number of studies have revealed cell surface receptors for these steroid binding proteins (1,(14)(15)(16)(17)(18). In the present study we have demonstrated the binding of TeBG by MCF-7 cells, which are known to be responsive to both androgens (22) and estrogens (43). These data include specific binding sites for TeBG on the cell surface, temperature-dependent latency, and movement through classic sub-cellular organelles involved in endocytosis.…”

Section: Discussionmentioning

confidence: 47%

Receptor-Mediated Endocytosis of an Extracellular Steroid-Binding Protein (TeBG) in MCF-7 Human Breast Cancer Cells*

et al. 1991

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Previous studies suggested that an extracellular steroid-binding protein, testosterone-estradiol-binding globulin (TeBG), can enter a variety of cells. Experiments were conducted to determine whether uptake of TeBG occurs by nonspecific fluid phase endocytosis or via a specific receptor-mediated process. In human breast carcinoma cells (MCF-7) maintained on serum-free medium, exposure to radiolabeled TeBG resulted in cellular uptake, which reached a plateau by 6 h and could be inhibited 80% by competition with unlabeled TeBG. Uptake was temperature dependent with cell-associated radioactivity at 37 C being 1.6-fold higher than at 4 C. Subsequent exposure of cells to pronase resulted in release of the cell-associated TeBG by 88% and 44% at 4 C and 37 C, respectively. After transfer to media devoid of TeBG, approximately 35% of cell-associated radioactivity was release into the medium at 37 C; it was not possible to distinguish whether this was released from the cell surface or from inside the cell. Investigation of the localization of TeBG-gold complexes by electron microscopy revealed that TeBG first binds to the plasmalemma. Within 15 min label appears in receptosomes, which fuse to form multivesicular endosomes. By 1 h all label is observed in multivesicular endosomes and lysosomes, most of which are in the Golgi zone. Localization of the internalized radioactivity using classical cell fractionation techniques showed it appears in a symmetrical band exhibiting the same buoyant density as the lysosomal marker acid phosphatase. The observations reported here show that: 1) TeBG binds to MCF-7 cells; 2) some of the bound TeBG is taken up via a mechanism with all the characteristics of receptor-mediated endocytosis; and 3) within these cells TeBG is localized in endosomes and lysosomes.

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Section: Discussionmentioning

confidence: 47%

Receptor-Mediated Endocytosis of an Extracellular Steroid-Binding Protein (TeBG) in MCF-7 Human Breast Cancer Cells*

et al. 1991

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“…1,25 In these cells, andro gens (T and DHT) exert antiestrogenic effects in inhibiting progesterone receptor synthesis. 66,67 Since this effect was blocked by antiandrogens, it was felt that this antiestrogenic effect occurred via the androgen receptor. 2 Studies have shown that 5α-reduced androgens at physiologic concentra tions can inhibit aromatase activity, 63 and in differ ent lines of human breast carcinoma cells there was a reciprocal relationship between aromatase and 5α-reductase activity 3 (Fig.…”

Section: Breast Carcinoma Tissuementioning

confidence: 99%

The Role of Peripheral Metabolism in Androgen Action

Killinger¹

1986

Semin Reprod Med

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Estrogen/progesterone treatment in adulthood affects the size of several components of the medial preoptic area in the male rat

Bloch¹,

Gorski²

1988

J of Comparative Neurology

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The results of preliminary studies suggested that steroid and/or propylthiouracil (PTU) treatment of adult gonadectomized (Gxd) male rats significantly reduced the volume of the sexually dimorphic nucleus of the preoptic area (SDN-POA). Therefore, we designed a study to examine this effect in detail. Groups of adult rats were sham Gxd (intact) or Gxd, then treated with multiple injections of oil (males and females), or estrogen and progesterone (males). Gonadectomized estrogen/progesterone-treated males had a significantly smaller SDN-POA volume, smaller volume of the medial division of the medial preoptic nucleus (MPNm), smaller volume of the anteroventral MPNm (MPNav), and larger volume of the anteroventral periventricular nucleus (AVPv). The volume of the central division of the medial preoptic nucleus (MPNc) or of the suprachiasmatic nucleus was not affected. There were no differences between Gxd estrogen/progesterone-treated males vs the group that received PTU as well, indicating that the PTU treatment was unnecessary. The reduced volume of the SDN-POA was due to a reduced volume of the MPNav and of the portion of the SDN-POA located within the MPNm-exclusive of the MPNav and MPNc. In conclusion, estrogen/progesterone treatment in adulthood caused significant changes in the volume of several medial preoptic structures in two separate groups of Gxd males. Because the steroids produced no significant effects in intact males, testicular hormones appear to "protect" these structures from the effects of the estrogen/progesterone treatment.

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Androgens inhibit estrogen action in MCF-7 human breast cancer cells

Cited by 32 publications

References 3 publications

Receptor-Mediated Endocytosis of an Extracellular Steroid-Binding Protein (TeBG) in MCF-7 Human Breast Cancer Cells*

Receptor-Mediated Endocytosis of an Extracellular Steroid-Binding Protein (TeBG) in MCF-7 Human Breast Cancer Cells*

The Role of Peripheral Metabolism in Androgen Action

Estrogen/progesterone treatment in adulthood affects the size of several components of the medial preoptic area in the male rat

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