ArticleMolecular cancer2017
Epigenetic down regulation of G protein-coupled estrogen receptor (GPER) functions as a tumor suppressor in colorectal cancer.
Article in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Intricate roles of estrogen and estrogen receptors in digestive system cancers: a systematic review.Cancer biology & medicine · 2024Pooled it
- Estradiol Reshapes Cell-Type-Dependent Basal Redox Set-Points in Colorectal Carcinoma Cells.Biomedicines · 2026Article
- Progress of estrogen receptor and splice variants in ovarian carcinoma.Journal of ovarian research · 2026Review
- Review
- Sex steroid receptors in colorectal cancer: implications for tumor progression, therapeutic opportunities, and sex-specific outcomes.Annals of medicine and surgery (2012) · 2026Review
- G-protein coupled estrogen receptor 1Frontiers in endocrinology · 2026Article
- Differences in the role of Gper1 in colorectal cancer progression depending on sex.Oncology letters · 2025Article
- LNS8801: An Enantiomerically Pure Agonist of the G Protein-Coupled Estrogen Receptor Suitable for Clinical Development.Cancer research communications · 2025Article
- Asparagine synthetase and G-protein coupled estrogen receptor are critical responders to nutrient supply in KRAS mutant colorectal cancer.International journal of cancer · 2025Article
- Interaction of GPER-1 with the endocrine signaling axis in breast cancer.Frontiers in endocrinology · 2025Review
- Natural Alkaloids in Cancer Therapy: Berberine, Sanguinarine and Chelerythrine against Colorectal and Gastric Cancer.International journal of molecular sciences · 2024Review
- Article
- 17β-estradiol in colorectal cancer: friend or foe?Cell communication and signaling : CCS · 2024Review
- The G-Protein-Coupled Estrogen Receptor Selective Agonist G-1 Attenuates Cell Viability and Migration in High-Grade Serous Ovarian Cancer Cell Lines.International journal of molecular sciences · 2024Article
- Correlation between the RNA Expression and the DNA Methylation of Estrogen Receptor Genes in Normal and Malignant Human Tissues.Current issues in molecular biology · 2024Article
- G protein-coupled estrogen receptor 1 and collagen XVII endodomain expression in human cutaneous melanomas: can they serve as prognostic factors?Pathology oncology research : POR · 2024Article
- Role of sex steroids in colorectal cancer: pathomechanisms and medical applications.American journal of cancer research · 2024Review
- Review
- Stimulatory Anticancer Effect of Resveratrol Mediated by G Protein-Coupled Estrogen Receptor in Colorectal Cancer.Biomolecules & therapeutics · 2023Article
- GPER: An Estrogen Receptor Key in Metastasis and Tumoral Microenvironments.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEstrogenic signals are suggested to have protection roles in the development of colorectal cancer (CRC). The G protein-coupled estrogen receptor (GPER) has been reported to mediate non-genomic effects of estrogen in hormone related cancers except CRC. Its expression and functions in CRC were investigated.
methodsThe expression of GPER and its associations with clinicopathological features were examined. The mechanisms were further investigated using cells, mouse xenograft models, and clinical human samples.
resultsGPER was significantly (p < 0.01) down regulated in CRC tissues compared with their matched adjacent normal tissues in our two cohorts and three independent investigations from Oncomine database. Patients whose tumors expressing less (n = 36) GPER showed significant (p < 0.01) poorer survival rate as compared with those with greater levels of GPER (n = 54). Promoter methylation and histone H3 deacetylation were involved in the down regulation of GPER in CRC cell lines and clinical tissues. Activation of GPER by its specific agonist G-1 inhibited proliferation, induced cell cycle arrest, mitochondrial-related apoptosis and endoplasmic reticulum (ER) stress of CRC cells. The upregulation of reactive oxygen species (ROS) induced sustained ERK1/2 activation participated in G-1 induced cell growth arrest. Further, G-1 can inhibit the phosphorylation, nuclear localization, and transcriptional activities of NF-κB via both canonical IKKα/ IκBα pathways and phosphorylation of GSK-3β. Xenograft model based on HCT-116 cells confirmed that G-1 can suppress the in vivo progression of CRC.
conclusionsEpigenetic down regulation of GPER acts as a tumor suppressor in colorectal cancer and its specific activation might be a potential approach for CRC treatment.
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