Breast cancer is a malignant tumor that occurs in the epithelial tissues of the breast gland. The cause of the disease is not fully understood and may be related to genetic, endocrine and other factors. For estrogen or progesterone receptor-positive early breast cancer, endocrine therapy is efficient, simple, and fewer side-effect, so endocrine therapy plays an important role in the treatment for early breast cancer. But most of them will develop drug-resistant after 8 to 14 months and have to combine with chemotherapy or molecule targeted therapy. However, there are still different ideas in the effects of endocrine therapy drugs alone or in combination with chemotherapy or molecule targeted drugs, pre-menopausally or post-menopausally.
Breast Neoplasms ; Humans ; Receptors, Estrogen

No abstract available.
Estrogens* ; Humans* ; Pituitary Neoplasms* ; Receptors, Estrogen*

No abstract available.
Breast Diseases* ; Breast* ; Estrogens* ; Progesterone* ; Receptors, Estrogen* ; Receptors, Progesterone*

Estrogen receptor (ER) and progesterone receptor (PR) are two important members of steroid receptors family, an evolutionarily conserved family of transcription factors. Upon binding to their ligands, ER and PR enter cell nucleus to interact with specific DNA element in the context of chromatin to initiate the transcription of diverse target genes, which largely depends on the timely recruitment of a wide range of cofactors. Moreover, the interactions between steroid hormones and their respective receptors also trigger post-translational modifications on these receptors to fine-tune their transcriptional activities. Besides the well-known phosphorylation modifications on tyrosine and serine/threonine residues, recent studies have identified several other covalent modifications, such as ubiquitylation and sumoylation. These post-translational modifications of steroid receptors affect its stability, subcellular localization, and/or cofactor recruitment; eventually influence the duration and extent of transcriptional activation. This review is to focus on the recent research progress on the transcriptional activation of nuclear ER and PR as well as their physiological functions in early pregnancy, which may help us to better understand related female reproductive diseases.
Ligands ; Phosphorylation ; Receptors, Estrogen ; Receptors, Progesterone ; Sumoylation ; Transcriptional Activation

Humans ; Female ; Receptors, Estrogen/metabolism* ; Breast Neoplasms/metabolism* ; Receptors, Progesterone/metabolism* ; Immunohistochemistry ; Estrogen Receptor alpha

One third of estrogens in the male are from the testis and the others from outside the testis. Aromatase P450 (CYP19) is an enzyme responsible for the conversion of androgens to estrogens. Estrogens regulate cell function via specific receptors--estrogen receptors (ER) which include ER alpha and ER beta. It has been found that the role of estrogens in male reproduction is complex and important, particularly during the neonatal life. Males lacking ER alpha are completely infertile because ER alpha-induced estrogens regulate the reabsorption of luminal fluid in the head of the epididymis and disruption of this essential function causes sperm to enter the epididymis diluted, rather than concentrated, resulting in infertility. Whereas males lacking aromatase or ER beta are fully fertile. Therefore, it is concluded that ER alpha, but not aromatase or ER beta, is essenitial for normal male fertility.
Animals ; Aromatase ; physiology ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Estrogens ; physiology ; Humans ; Male ; Receptors, Estrogen ; physiology ; Reproduction ; physiology

Estrogen plays an important role in the regulation of male reproduction. Through binding with the estrogen receptor (ER), estrogen produces genomic and non-genomic effects. Estrogen receptors include ERalpha and ERbeta which distribute in the male reproductive system including the testis, epididymis, prostate and penis. The spermatogenesis is impaired in mice with ERalpha gene knockout; however, it remains normal in mice with ERbeta gene knockout. This phenomenon suggests that the two subtypes of ER play different roles in spermatogenesis. Moreover, ERalpha or ERbeta may also act as a substitute of another.
Animals ; Estrogen Receptor alpha ; metabolism ; Estrogen Receptor beta ; metabolism ; Genitalia, Male ; metabolism ; Male ; Mice ; Receptors, Estrogen ; metabolism

OBJECTIVETo study the expression of the estrogen receptor (ER) and type II collagen in the mandibular condylar cartilage of the human embryo.

METHODSThe expression and localization of ERalpha, ERbeta, and type II collagen in the mandibular condylar cartilage of the human embryo were examined through hematoxylin-eosin (HE) and immunohistochemistry staining.

RESULTSType II collagen was primarily localized in the transitional and hypertrophic layers of the condylar cartilage. ERa was mostly expressed in the transitional and hypertrophic cartilaginous layers of the condylar cartilage. ERa was evenly distributed in the cell, whereas ERbeta was localized in the nuclei. No expression of type II collagen and ER was found in the fibrage and the proliferative layer although minimal expression was found in the calcified cartilage.

CONCLUSIONThe distribution of ER and type II collagen in the mandibular condylar cartilage was consistent. Estrogen can selectively combine with different subtypes of ER that regulate the ability of the condylar cartilage cells to secrete type II collagens.

No abstract available.
Estrogens* ; Humans ; Receptors, Estrogen* ; Thyroid Diseases* ; Thyroid Gland*

Estrogen is a strong growth regulator of the prostate stromal cells, it produces a marked effect by means of binding to specific receptors. Many researches have indicated that estrogen and estrogen receptors take part in the whole process and development of benign prostatic hyperplasia. This article gives a general description of the function of estrogen and estrogen receptors in benign prostatic hyperplasia.
Estrogens ; physiology ; Humans ; Male ; Prostatic Hyperplasia ; metabolism ; Receptors, Estrogen ; physiology