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Updated: Jun 12, 2026

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
Published on: February 21, 2014
Estrogen receptor {beta}1 expression is regulated by miR-92 in breast cancer
Hakeemah Al-Nakhle1, Philip A Burns, Michele Cummings
1Leeds Institute of Molecular Medicine, University of Leeds, Leeds, United Kingdom.
Abstract:
Estrogen receptor beta1 (ERbeta1) downregulation occurs in many breast cancers, but the responsible molecular mechanisms remain unclear. Here, we report that levels of ERbeta1 expression are negatively regulated by the microRNA miR-92. Expression analysis in a cohort of primary breast tumors confirmed a significant negative correlation between miR-92 and both ERbeta1 mRNA and protein. Inhibition of miR-92 in MCF-7 cells increased ERbeta1 expression in a dose-dependent manner, whereas miR-92 overexpression led to ERbeta1 downregulation. Reporter constructs containing candidate miR-92 binding sites in the 3'-untranslated region (UTR) of ERbeta1 suggested by bioinformatics analysis confirmed that miR-92 downregulated ERbeta1 via direct targeting of its 3'-UTR. Our results define a potentially important mechanism for downregulation of ERbeta1 expression in breast cancer.
Insights
MicroRNA miR-92 directly targets the estrogen receptor beta1 (ERbeta1) 3'-untranslated region, leading to ERbeta1 downregulation in breast cancer. This microRNA (miRNA) pathway is a key mechanism behind reduced ERbeta1 expression in tumors.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Estrogen receptor beta1 (ERbeta1) downregulation is common in breast cancer.
- The molecular mechanisms driving ERbeta1 loss remain largely unknown.
Purpose of the Study:
- To investigate the role of microRNA miR-92 in regulating ERbeta1 expression in breast cancer.
- To elucidate the molecular mechanism by which miR-92 affects ERbeta1 levels.
Main Methods:
- Expression analysis in primary breast tumors.
- In vitro experiments using MCF-7 cells (miR-92 inhibition and overexpression).
- Bioinformatics analysis and reporter assays to confirm direct targeting of the ERbeta1 3 -untranslated region (UTR).
Main Results:
- A significant negative correlation was observed between miR-92 levels and both ERbeta1 mRNA and protein in breast tumors.
- Inhibition of miR-92 in MCF-7 cells resulted in a dose-dependent increase in ERbeta1 expression.
- Overexpression of miR-92 led to ERbeta1 downregulation, confirming direct targeting of the ERbeta1 3 -UTR by miR-92.
Conclusions:
- MicroRNA miR-92 directly targets the 3 -UTR of ERbeta1, leading to its downregulation.
- This miR-92-mediated downregulation represents a significant molecular mechanism contributing to reduced ERbeta1 expression in breast cancer.
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