The regulatory role of estrogens and nuclear estrogen receptors, i. e., estrogen receptor α and β has been reported in gastrointestinal diseases. However, the contribution of G protein-coupled estrogen receptor, the membrane-bound estrogen receptor, is still poorly understood. Unlike nuclear estrogen receptors, which are responsible for the genomic activity of estrogens, the G protein-coupled estrogen receptor affects the "rapid" non-genomic activity of estrogens, leading to modulation of many signaling pathways and ultimately changing gene expression. Recently, the crucial role of G protein-coupled estrogen receptor in intestinal pathogenesis has been documented. It has been shown that the G protein-coupled estrogen receptor can modulate the progression of irritable bowel syndrome, inflammatory bowel diseases such as Crohn's disease and ulcerative colitis as well as colorectal cancer. The G protein-coupled estrogen receptor appears to be a potent factor regulating abdominal sensitivity and pain, intestinal peristalsis, colitis development, proliferation and migration potential of colorectal cancer cells and seems to be a useful target in gastrointestinal diseases. In this review, we present the current state of knowledge about the contribution of the G protein-coupled estrogen receptor to irritable bowel syndrome, inflammatory bowel diseases and colorectal cancer.
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http://dx.doi.org/10.3389/fendo.2020.00390 | DOI Listing |
Breast Cancer Res
January 2025
Department of Cancer Biology, Loyola University Chicago Stritch School of Medicine, Maywood, IL, 50153, USA.
Resistance to endocrine therapies remains a major clinical hurdle in breast cancer. Mutations to estrogen receptor alpha (ERα) arise after continued therapeutic pressure. Next generation selective estrogen receptor modulators and degraders/downregulators (SERMs and SERDs) show clinical efficacy, but responses are often non-durable.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Oncology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17 Yongwaizheng Street, Nanchang, 330006, Jiangxi Province, China.
The benefit of adjuvant chemotherapy (CT) for hormone receptor-negative T1a and T1bN0M0 breast cancer remains uncertain. Our study was to explore prognostic value and identify candidates of adjuvant CT for these patients. The data of hormone receptor-negative T1a and T1bN0M0 breast cancer patients were extracted from the Surveillance, Epidemiology, and End Results (SEER) database from 2010 to 2015.
View Article and Find Full Text PDFEnviron Pollut
January 2025
Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, People's Republic of China; NHC Key Laboratory of Etiology and Epidemiology(Harbin Medical University); Joint Key Laboratory of Endemic Diseases(Harbin Medical University, Guizhou Medical University, Xi'an Jiaotong University); Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, People's Republic of China. Electronic address:
Background: Skeletal fluorosis is a chronic metabolic bone disease caused by excessive accumulation of fluoride in the bones. Previous studies have found that when the intake of tea fluoride is similar, the prevalence of skeletal fluorosis varies greatly among different ethnic groups, which may be related to different genetic backgrounds. Single nucleotide polymorphisms (SNPs) of estrogen receptor 1 (ESR1) and collagen type 1 α1 (COL1A1) were strongly associated with bone metabolism as well as bone growth and development, but their association with the risk of skeletal fluorosis has not been reported.
View Article and Find Full Text PDFEcotoxicol Environ Saf
January 2025
Department of Stomatology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, No. 242, Guangji Road, Suzhou, Jiangsu Province 215000, China. Electronic address:
Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in utero can result in osteogenic defect during palatogenesis, but the effects on other craniofacial bones and underlying mechanisms remain to be characterized. By treating pregnant mice with TCDD (40 μg/kg) at the vital craniofacial patterning stages (embryonic day 8.5, 10.
View Article and Find Full Text PDFRSC Med Chem
December 2024
State Key Laboratory of Biocatalysis and Enzyme Engineering, National & Local Joint Engineering Research Center of High-throughput Drug Screening Technology, School of Life Sciences, Hubei University Wuhan 430062 China
Despite the success of endocrine therapies in treating ER-positive breast cancer, the development of resistance remains a significant challenge. Estrogen receptor targeting proteolysis-targeting chimeras (ER PROTACs) offer a unique approach by harnessing the ubiquitin-proteasome system to degrade ER, potentially bypassing resistance mechanisms. In this review, we present the drug design, efficacy and early clinical trials of these ER PROTACs.
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