Breast cancer is one of the most common malignancies worldwide and is responsible for a high mortality rate. However, the underlying pathological mechanism of breast cancer remains unclear. MicroRNAs (miRNAs/miRs) play critical roles in the progression of breast cancer. Recent studies have reported that miR-124/CD151 participates in the development of breast cancer. However, the exact molecular mechanism of miR-124/CD151 action in 17β-estradiol (E2)-treated breast cancer cells remains unknown. Thus, the present study aimed to investigate miR-124 and CD151 expression levels in MCF-7 cells treated with E2 via reverse transcription-quantitative PCR and western blot analyses. Bioinformatic analysis was performed to predict and identify whether CD151 is a potential target of miR-124. The Cell Counting Kit-8 and colony formation assays were performed to detect proliferation of MCF-7 cells. In addition, the invasive and migratory abilities of MCF-7 cells were assessed via the Transwell and wound healing assays, respectively. The results demonstrated that E2 downregulated miR-124 expression, while upregulating G protein -coupled estrogen receptor (GPER) expression in MCF-7 cells. Following treatment with the GPER antagonist, G15, miR-124 expression was significantly enhanced and E2-induced proliferation, invasion and migration of MCF-7 cells were notably inhibited. In addition, CD151 was confirmed as a direct target of miR-124. CD151 silencing remarkably suppressed the proliferation, invasion and migration of E2-induced MCF-7 cells. Taken together, these results suggest that upregulation of GPER expression induced by E2 promotes proliferation, invasion and migration of breast cancer cells by regulating the miR-124/CD151 pathway. Thus, the results of the present study provide a potential novel method for the treatment and prognosis of breast cancer.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.