ArticleExperimental and therapeutic medicine2017
miR-148a Suppresses estrogen-induced viability and migration of breast cancer cells via inhibition of estrogen receptor α expression.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Integrating bulk and single cell sequencing data to identify prognostic biomarkers and drug candidates in HBV associated hepatocellular carcinoma.Scientific reports · 2025Article
- Evaluation of Serum MicroRNAs (miR-9-5p, miR-17-5p, and miR-148a-3p) as Potential Biomarkers of Breast Cancer.BioMed research international · 2022Article
- Perspectives on the Role of Non-Coding RNAs in the Regulation of Expression and Function of the Estrogen Receptor.Cancers · 2020Review
- Plasma-based microRNA signatures in early diagnosis of breast cancer.Molecular genetics & genomic medicine · 2020Article
- Overexpression of miR-148a inhibits viability and invasion of ovarian cancer OVCAR3 cells by targeting FOXO3.Oncology letters · 2019Article
- G protein-coupled estrogen receptor mediates anti-inflammatory action in Crohn's disease.Scientific reports · 2019Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRs) play critical roles in the development and malignant progression of human cancers. miR-148a has previously been found to inhibit the migration and invasion of breast cancer cells. However, the underlying mechanism of miR-148a in regulating the viability and migration of estrogen receptor (ER) α-positive breast cancer cells is still unknown. In this study, ERα-positive breast cancer MCF7 cells were treated with estradiol (E2). Data from MTT and wound healing assays showed that E2 treatment promoted the viability and migration of MCF7 cells. A bioinformatics analysis and luciferase reporter assay identified ERα as a direct target of miR-148a. Ectopic expression of miR-148a significantly decreased the protein expression of ERα (P<0.01), while knockdown of miR-148a significantly increased the ERα protein level in MCF7 cells (P<0.01). Furthermore, miR-148a overexpression significantly inhibited the E2-induced viability and migration of MCF7 cells (P<0.01), similar to the effect of silencing ERα. However, overexpression of ERα rescued the suppressed viability and migration caused by miR-148a upregulation. Finally, it was found that E2 treatment led to a significant decrease in the miR-148a level in MCF7 cells (P<0.01). These results suggest that miR-148a can suppress the E2-induced viability and migration of MCF7 breast cancer cells via inhibition of ERα protein expression, expanding the understanding of miR function in ERα-positive breast cancer.
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