Gonadotropin-releasing hormone receptor inhibits triple-negative breast cancer proliferation and metastasis

• Published in: Journal of international medical research Vol. 50; no. 3; p. 3000605221082895
• Main Authors: Chen, Cai-Ping, Lu, Xiang
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.03.2022; Sage Publications Ltd; SAGE Publishing
• Subjects: Apoptosis; Breast cancer; Cell cycle; Cell growth; Cell Line, Tumor; Cell Movement; Cell Proliferation; Humans; Medical prognosis; Metastasis; Pre-Clinical Research Report; Protein expression; Receptors, LHRH - genetics; Receptors, LHRH - metabolism; Triple Negative Breast Neoplasms - drug therapy; Triple Negative Breast Neoplasms - genetics; Triple Negative Breast Neoplasms - metabolism; apoptosis; triple-negative breast cancer; proliferation; metastasis; prognosis; Gonadotropin-releasing hormone receptor
• ISSN: 0300-0605; 1473-2300
• DOI: 10.1177/03000605221082895

Background Gonadotropin-releasing hormone receptor (GnRHR) is expressed in several malignant tumors and inhibits the proliferation and metastasis of cancer cells, but its role in triple-negative breast cancers (TNBCs) is unclear. This study investigated the biological effects of GnRHR and their influence on TNBC prognosis. Methods The GSE21653 database was used to obtain information about GnRHR expression and clinicopathological factors in patients with TNBC. GnRHR was activated in cultured MDA-MB-231 and MDA-MB-468 cells by leuprolide acetate and antagonized by elagolix sodium. Cell proliferation was assessed by the cell counting kit-8 and colony formation assays. Cell metastasis was detected by the wound healing assay and Transwell assay. Apoptosis and the cell cycle were investigated by flow cytometry. GnRHR protein expression was determined by western blotting. Results GnRHR mRNA expression was significantly higher in patients with TNBC than in hormone receptor+/human epidermal growth factor receptor (HER)2– and HER2+ patients with breast cancer. Patients with high GnRHR expression had significantly better disease-free survival than those with lower expression. Activated GnRHR significantly inhibited cell proliferation and metastasis, increased apoptosis, and enhanced GnRHR protein expression levels. Conclusion GnRHR inhibits TNBC proliferation and metastasis, suggesting it could be targeted for TNBC treatment.