Abstract
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.
Highlights
The G protein-coupled estrogen receptor (GPER, previously known as GPR30) is a seventransmembrane receptor discovered, among others, in breast cancer tissue and estrogen receptorpositive MCF-7 cell line [1,2,3,4,5,6,7]
We summarize the evidence for GPER expression and function in the pathophysiology of intestinal diseases, i.e., irritable bowel syndrome, inflammatory bowel diseases and colorectal cancer
At the molecular level GPER appears to be engaged in the modulation of signaling pathway of extracellular signal-regulated kinases (ERKs), which leads to changes in expression of immune-related genes which was documented in the intestine of inflammatory bowel disease (IBDs) patients and murine model
Summary
The G protein-coupled estrogen receptor (GPER, previously known as GPR30) is a seventransmembrane receptor discovered, among others, in breast cancer tissue and estrogen receptorpositive MCF-7 cell line [1,2,3,4,5,6,7]. In contrast to nuclear ERs, which predominantly regulate expression of target genes through direct interaction with estrogen response element or indirectly through transcription factors, GPER is responsible for “rapid” non-genomic activity of estrogens, leading to modulation of many signaling pathways and gene expression. It was found that GPER is capable to affect nuclear factor-κB (NF-κB) and Notch as well as Hippo signaling, where the membrane-bound estrogen receptor regulates phosphorylation of crucial proteins through Gαq−11 action, enhancing the proliferation and migration potential of breast cancer cells [11, 13, 14]. We summarize the evidence for GPER expression and function in the pathophysiology of intestinal diseases, i.e., irritable bowel syndrome, inflammatory bowel diseases and colorectal cancer
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