• Title, Summary, Keyword: estrogen

Search Result 1,228, Processing Time 0.075 seconds

Estrogen Modulation of Human Breast Cancer Cell Growth

  • Lee, Hyung-Ok;Sheen, Yhun-Yhong
    • Archives of Pharmacal Research
    • /
    • v.20 no.6
    • /
    • pp.566-571
    • /
    • 1997
  • To gain further insight into how estrogens modulate cell function, the effects of estrogen on cell proliferation were studied inhuman breast cancer cells. We examined the effects of estrogen on the proliferation of three human breast cancer cell lines that differed in their estrogen receptor contents. Ten nM estradiol markedly stimulated the proliferation of MCF-7 human breast cancer cells that contained high levels of estrogen receptor $1.15{\pm}0.03 pmole/mg protein)$(over that of control. In T47D cells that contained low levels of estrogen receptor $0.23{\pm}0.05 pmole/mg protein)$, Ten nM estrogen slightly stimulated the proliferation over that of control. MDA-MB-231 cells, that contained no detectable levels of estrogen receptors, had their growth unaffected by estrogen. These results showed their sensitivity to growth stimulation by estrogen correlated well with their estrogen receptor content. Also we examined the effect of estrogen on cellular progesterone receptor level as well as plasminogen activator activity in MCF-7 cells. Ten nM estradiol showed maximal stimulation of progesterone receptor level as well as plasminogen activator activity in MCF-7 cells. It is not clear whether these stimulations of progesterone receptor and plasminogen activator activity by estrogen are related to the estrogen stimulation of cell proliferation of MCF-7 cells. Studies with estrogen in human breast cancer cells in culture indicate that sensitivity to growth stimulation by estrogen correlates well with estrogen receptor contents.

  • PDF

Immunohistochemical application of anti-proliferating cell nuclear antigen antibody on the development of uterus following sex hormone administration in rats (성 hormone이 rat 자궁 발달에 미치는 영향에 대한 proliferating cell nuclear antigen 항체의 면역조직학적 응용)

  • Koh, Phil-ok;Kwak, Soo-dong
    • Korean Journal of Veterinary Research
    • /
    • v.37 no.2
    • /
    • pp.281-289
    • /
    • 1997
  • The study was designed to investigate the effects of progesterone and estrogen on the uterus of rats by immunohistochemical methods using Proliferating Cell Nuclear Antigen (PCNA) antibody. Eighteen female rats(Wistar), weighing initially about 300g, were ovariectomized. These rats were divided into four groups, progesterone-treated group, estrogen-treated group, estrogen+progesterone-treated group, and control group, progesterone-treated group was injected with 1mg of progesterone per rat per day for 2 days and estrogen-treated group with $20{\mu}g$ of $17{\beta}-estradiol$ for 3 days and estrogen+progesterone-treated group with $17{\beta}-estrdiol$ for 3 days and then with progesterone for 2 days as above. In gross findings, the uteri were markedly hypertrophied by estrogen treatment but were not affect in size by progesterone treatment. Immunohistochemical investigation was performed on the cell types with higher appearance of PCNA positive reaction cells in four groups. The groups with higher appearance of the stromal cells were ordered as estrogen-treated group, progesterone-treated group, estrogen+progesterone-treated group, and control group. The muscle cells were ordered as progesterone-treated group, estrogen-treated group, estrogen+progesterone-treated group, and control group. Positive reaction cells of the stromal cells were total 4.6 times higher than those of muscle cells. Therefore, the affect of the hypertrophy on the uterus by estrogen was larger than those of progesterone and affect on the uterus by stromal cells were larger than those of muscle cells. The group with more PCNA positive reaction cells of luminal epithelial cells were ordered as control group, progesterone-treated group, estrogen+progesterone-treated group, and estrogen-treated group, and glandular epithelial cells were ordered as estrogen+progesterone-treated group, progesterone-treated group, control group, and estrogen-treated group. It was suggested that estrogen and progesterone did not affect on the proliferating cells of luminal epithelial cells and affection of progesterone on the development of glandular epithelial cell was larger than that of estrogen.

  • PDF

Role of G Protein-Coupled Estrogen Receptor in Cancer Progression

  • Jung, Joohee
    • Toxicological Research
    • /
    • v.35 no.3
    • /
    • pp.209-214
    • /
    • 2019
  • Cancer is the leading cause of mortality worldwide. In cancer progression, sex hormones and their receptors are thought to be major factors. Many studies have reported the effects of estrogen and estrogen receptors (ERs) in cancer development and progression. Among them, G protein-coupled estrogen receptor (GPER), a G protein-coupled receptor, has been identified as an estrogen membrane receptor unrelated to nuclear ER. The mechanism of GPER, including its biological action, function, and role, has been studied in various cancer types. In this review, we discuss the relation between GPER and estrogen or estrogen agonists/antagonists and cancer progression.

Antiestrogen Interaction with Estrogen Receptors and Additional Antiestrogen Binding sites in Human Breast Cancer MCF-7 Cells

  • Ahn, Mee-Ryung;Sheen, Yhun-Yhong
    • Archives of Pharmacal Research
    • /
    • v.20 no.6
    • /
    • pp.579-585
    • /
    • 1997
  • To gain further insight into the mechanism of action of antiestrogens, we examined the interaction of antiestrogen with the estrogen receptor system and with estrogen- noncompetable antiestrogen binding sites. In addition to binding directly to the estrogen receptor, antiestrogens can be found associated with binding sites that are distinct from the estrogen receptor. In contrast to the restriction of estrogen receptors to estrogen target cells, such as those of uterus and mammary glands, antiestrogen binding sites are present in equal amounts in estrogen receptor-positive and -negative human breast cancer cell lines, such as MCF-7, T47D, and MDA-MB-231 that differ markedly in their sensitivity to antiestrogens. In order to gain greater insight into the role of these antiestrogen binding sites in the action of antiestrogens, we have examined the biopotency of different antiestrogens for the antiestrogen binding sites and that is CI628 > tamoxifen > trans-hydroxy tamoxifen > CI628M > H1285 > LY117018. This order of affinities does not parallel the affinity of these compounds for the estrogen receptor nor the potency of these compounds as antiestrogens. Indeed, compounds with high affinity for the estrogen receptor and greatest antiestrogenic potency have low affinities for these antiestrogen binding sites. Antiestrogenic potency correlates best with estrogen receptor affinity and not with affinity for antiestrogen binding sites. In summary, our findings suggested that interaction with the estrogen receptor is most likely the mechanism through which antiestrogens evoke their growth inhibitory effects.

  • PDF

Effects of $17{\beta}$-Estradiol and Estrogen Receptor Antagonists on the Proliferation of Gastric Cancer Cell Lines

  • Kim, Myung-Jin;Cho, Sung-Il;Lee, Kun-Ok;Han, Hyung-Joon;Song, Tae-Jin;Park, Seong-Heum
    • Journal of Gastric Cancer
    • /
    • v.13 no.3
    • /
    • pp.172-178
    • /
    • 2013
  • Purpose: The aims of this study were as follow: 1) to de scribe the expression status of estrogen receptor-${\alpha}$ and -${\beta}$ mRNAs in five gastric carcinoma cell lines; 2) to evaluate in vitro the effects of $17{\beta}$-estradiol and estrogen receptor antagonists on the proliferation of the cell lines. Materials and Methods: Detection of estrogen receptor-${\alpha}$ and estrogen receptor-${\beta}$ mRNA in five human gastric cancer cell lines (AGS, KATO III, MKN28, MKN45 and MKN74) was made by the reverse transcription-polymerase chain reaction system. To evaluate the effect of $17{\beta}$-estradiol and estrogen receptor antagonists on the proliferation of gastric cancer cell line, the cell lines which expressed both es trogen receptors were chosen and treated with $17{\beta}$-estradiol and estrogen receptor antagonists (methyl-piperidino-pyrazole and pyrazolo [1,5-a] pyrimidine). Cell proliferation was assessed with the methylthiazol tetrazolium test. Results: Estrogen receptor-${\alpha}$ and estrogen receptor-${\beta}$ mRNAs were expressed in three (KATO III, MKN28 and MKN45) and all of the five gastric cancer cell lines, respectively. At higher concentrations, $17{\beta}$-estradiol inhibited cell growth of MKN28, MKN45 and KATO III cell lines. Neither estrogen receptor-${\alpha}$ nor estrogen receptor-${\beta}$ antagonist blocked the anti-proliferative effect of $17{\beta}$-estradiol. Conclusions: Our results indicate that estrogen receptor-${\beta}$ mRNAs are preferentially expressed in gastric cancers and also imply that hormone therapy rather than estrogen receptor blockers may be a useful strategy for the treatment of estrogen receptor-${\beta}$ positive gastric cancer. Its therapeutic significance in gastric cancer are, however, limited until more evidence of the roles of estrogen receptors in the gastric cancer are accumulated.

The Effect of Combined Estrogen/calcium Therapy on Bone Metabolism in Ovariectomized Rats II. A Study on Metabolism of calcium, Phosphorus and Nitrogen in Ovariectomized Rats (에스트로겐/칼슘 혼합요법이 난소절제 쥐의 골대사에 미치는 영향 II. 칼슘, 인 및 질소대사에 관한 연구)

  • 이경화;오승호
    • Journal of the Korean Society of Food Science and Nutrition
    • /
    • v.25 no.6
    • /
    • pp.1006-1015
    • /
    • 1996
  • This study was carried out to investigate the effects of dietary calcium-salt, estrogen-treatment, and estrogen/calcium treatment on calcium, phosphorus and nitrogen metabolism. Female Sprague-Dawley rats with a body weight of 250~280g were underwent ovariectomy or sham-operation. The ovariectomized rats were divided into 9 different experimental groups including the saline-treated group, the estrogen-treated group, the high calcium salt-treated group, and the estrogen/calcium treated groups and fed for 6 weeks. Each group daily intake and excretion of calcium, phosphorus and nitrogen were measured and apparent digestibility and balance were also studied. The results were as follows: The excretion level of winn calcium was significantly higher the ovariectomized rats than the sham-operation group(p<0.01) and reduced with estrogen treatment but this difference was not statistically significant. Fecal loss of calcium was higher the ovariectomized rats than the sham-operation group(p<0.001). When the estrogen was treated, fecal loss was decreased and then apparent digestibility of calcium was increased. Calcium balance was significantly higher the high calcium treated groups than the control diet groups. The excretion level of urinary Phosphorus was higher the ovariectomized rats than sham-operation group, while these showed to be decreased in the calcium salt, the estrogen and the estrogen/calcium treated groups(p<0.01). Fecal loss of phosphrous was higher in the ovariectomized rats. When the estrogen was treated, the fecal loss was decreased in the avariectomized rat than that of other groups. The excretion level of urinary nitrogen was higher the ovariectomized rats than the sham-operation, while these showed to be decreased in the estrogen, the estrogen/calcium, and the estrogen gradually reduction/calcium intensification. Fecal loss of nitrogen was decreased in tile estrogen treated group. The results in this study showed that high calcium, estrogen/calcium and estrogen gradually reduction/calcium intensification in the ovariectomized rats enhanced calcium balance compared to the ovariectomized rats without calcium treatment, but little effects on the phosphorus and nitrogen balance.

  • PDF

Role of estrogen and RAS signaling in repeated implantation failure

  • Hong, Kwonho;Choi, Youngsok
    • BMB Reports
    • /
    • v.51 no.5
    • /
    • pp.225-229
    • /
    • 2018
  • In humans, hormonal regulation is crucial for the preparation of uterine environment leading to either successful implantation or menstrual cycle. Estrogen is a pivotal female steroid hormone that regulates the uterine dynamics along with progesterone in the estrous and menstrual cycles in humans. Estrogen signals act via nuclear estrogen receptor or membrane-bound receptor. The membrane-bound estrogen receptor plays a crucial role in the rapid response of estrogen in the uterine epithelium. Recently, RASD1 has received attention as a novel signal transducer of estrogen in various systems including female reproductive organs. In this review, we discuss the regulation of estrogen and RASD1 signaling in the uterus and also provide insights into RAS as a novel signaling molecule in repeated implantation failure.

A Study of Estrogen only Therapy and Estrogen Plus Androgen Combination Therapy in Surgical Menopause Patients (난소적출술 환자에서 Estrogen 단독요법 및 Estrogen-androgen 병합요법에 관한 연구)

  • Bai, Kwang-Bum
    • Clinical and Experimental Reproductive Medicine
    • /
    • v.29 no.4
    • /
    • pp.279-285
    • /
    • 2002
  • Objective : To evaluate the difference between estrogen only therapy and estrogen-androgen combination therapy in surgical menopause patients. Materials and Method: Surgical menopause patients received 0.625 mg conjugated equine estrogens or 0.625 mg conjugated equine estrogens plus 1.25 mg methyltestosterone for 2 years. Bone mineral density, menopausal symptoms, lipoprotein profiles were measured. Results: Both groups showed increased bone mineral density. In the combination group, total cholestero l, high density lipoprotein cholesterol and triglycerides decreased. In the estrogen only group, low density lipoprotein cholesterol decreased but high density lipoprotein cholesterol increased significantly. In both groups, menopausal symptoms were much improved. Side effects were easily tolerated in both groups. Conclusions: Estrogen-androgen combination therapy had comparable benefits compared with estrogen only therapy.

Dual roles of estrogen metabolism in mammary carcinogenesis

  • Chang, Min-Sun
    • BMB Reports
    • /
    • v.44 no.7
    • /
    • pp.423-434
    • /
    • 2011
  • A female hormone, estrogen, is linked to breast cancer incidence. Estrogens undergo phase I and II metabolism by which they are biotransformed into genotoxic catechol estrogen metabolites and conjugate metabolites are produced for excretion or accumulation. The molecular mechanisms underlying estrogen-mediated mammary carcinogenesis remain unclear. Cell proliferation through activation of estrogen receptor (ER) by its agonist ligands and is clearly considered as one of carcinogenic mechanisms. Recent studies have proposed that reactive oxygen species generated from estrogen or estrogen metabolites are attributed to genotoxic effects and signal transduction through influencing redox sensitive transcription factors resulting in cell transformation, cell cycle, migration, and invasion of the breast cancer. Conjuguation metabolic pathway is thought to protect cells from genotoxic and cytotoxic effects by catechol estrogen metabolites. However, methoxylated catechol estrogens have been shown to induce ER-mediated signaling pathways, implying that conjugation is not a simply detoxification pathway. Dual action of catechol estrogen metabolites in mammary carcinogenesis as the ER-signaling molecules and chemical carcinogen will be discussed in this review.

Ginsenoside-Rb1 Acts as a Weak Estrogen Receptor Agonist Independent of Ligand Binding.

  • Park, Wan-Kyu;Jungyoon Cho;Lee, Young-Joo
    • Proceedings of the Korean Society of Applied Pharmacology
    • /
    • /
    • pp.114-114
    • /
    • 2003
  • Ginseng is a medicinal herb widely used in Asian countries, and its pharmacological effects has been demonstrated in various systems such as cardiovascular, central nervous, and endocrine systems. Its effects are mainly attributed to the ginsenosides. We hypothesize that a component of Panax ginseng, ginsenoside-Rbl, acts by binding to estrogen receptor. We have investigated the estrogenic activity of ginsenoside-Rbl in a transient transfection system using estrogen receptors ${\alpha}$ or ${\beta}$ with estrogen -responsive luciferase plasmids in COS monkey kidney cells. Ginsenoside-Rbl activated both estrogen receptors ${\alpha}$ and ${\beta}$ in a dose-dependent manner (0.5 -100 M ). Activation was inhibited by the specific estrogen receptor antagonist ICI 182,780, indicating that the estrogenic effect of ginsenoside-Rbl is estrogen receptor dependent. Next, we evaluated the ability of ginsenoside-Rbl to induce estrogen-responsive progesterone receptor gene by semi-quantitative RT-PCR assays. MCF-7 cells treated with l7${\beta}$-estradiol or ginsenoside- Rb1 exhibited an increased expression of progesterone receptor mRNA. However, ginsenoside-Rbl failed to displace the specific binding of [3H]17${\beta}$-estradiol to estrogen receptor in MCF-7 cells as examined by whole cell ligand binding assays, suggesting that there is no direct interaction of ginsenoside-Rbl with estrogen receptor. Our results indicate that estrogen-like activity of ginsenoside-Rbl is independent of direct estrogen receptor association.

  • PDF