ArticleBreast cancer research : BCR2014
Identification of miR-26 as a key mediator of estrogen stimulated cell proliferation by targeting CHD1, GREB1 and KPNA2.
Article in Breast cancer research : BCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 110 citations in OpenAlex.
- Three ct-miRNA signature predicts disease outcome in early breast cancer women.Breast cancer research : BCR · 2026Article
- Altered microRNA profiles and associated pathways in canine mammary adenocarcinoma.Scientific reports · 2025Article
- Rat somatic genome editing enables ER+ breast cancer modeling.bioRxiv : the preprint server for biology · 2025Article
- Article
- Chromatin remodeling complexes: architects influencing breast cancer progression.Frontiers in cell and developmental biology · 2025Review
- The therapeutic potential of targeting the CHD protein family in cancer.Pharmacology & therapeutics · 2024Review
- MiR-101-3p targets KPNA2 to inhibit the progression of lung squamous cell carcinoma cell lines.Histology and histopathology · 2023Article
- CHD1, a multifaceted epigenetic remodeler in prostate cancer.Frontiers in oncology · 2023Review
- Construction of shared gene signature between rheumatoid arthritis and lung adenocarcinoma helps to predict the prognosis and tumor microenvironment of the LUAD patients.Frontiers in molecular biosciences · 2023Article
- The prognostic value of the GPAT/AGPAT gene family in hepatocellular carcinoma and its role in the tumor immune microenvironment.Frontiers in immunology · 2023Article
- Circulating Small EVs miRNAs as Predictors of Pathological Response to Neo-Adjuvant Therapy in Breast Cancer Patients.International journal of molecular sciences · 2022Article
- microRNA-26b inhibits growth and cellular invasion of ovarian cancer cells by targeting estrogen receptor α.3 Biotech · 2022Article
- Lipid Metabolism in Cancer: The Role of Acylglycerolphosphate Acyltransferases (AGPATs).Cancers · 2022Review
- Circulating non-coding RNAs as a diagnostic and management biomarker for breast cancer: current insights.Molecular biology reports · 2022Review
- Intrarenal Single-Cell Sequencing of Hepatitis B Virus Associated Membranous Nephropathy.Frontiers in medicine · 2022Article
- Sentinels of chromatin: chromodomain helicase DNA-binding proteins in development and disease.Genes & development · 2021Review
- Multiple-Molecule Drug Design Based on Systems Biology Approaches and Deep Neural Network to Mitigate Human Skin Aging.Molecules (Basel, Switzerland) · 2021Article
- Obesity, leptin, and deregulation of microRNA in lipid metabolisms: their contribution to breast cancer prognosis.Diabetology & metabolic syndrome · 2021Review
- Tumor Suppressor miRNA in Cancer Cells and the Tumor Microenvironment: Mechanism of Deregulation and Clinical Implications.Frontiers in oncology · 2021Review
- Potential miRNAs for miRNA-Based Therapeutics in Breast Cancer.Non-coding RNA · 2020Review
5 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionEstrogen signaling is pivotal in the progression of estrogen receptor positive breast cancer primarily by the regulation of cell survival and proliferation. Micro (mi)RNAs have been demonstrated to be regulated by estrogen to mediate estrogenic effects. Herein, we determined the role of estrogen regulated miR-26 and its underlying molecular mechanisms associated with estrogen receptor (ER)+ breast cancer proliferation.
methodsThe expression of miR-26a and miR-26b was evaluated by real-time quantitative (RT)-PCR. The expression of miR-26a or miR-26b was modulated in ER+ breast cancer cells (MCF-7 and T47D) and tumor cell growth in vitro and an in vivo xenograft model was determined. Bioinformatics analyses were utilized to screen for estrogen responsive genes, which were also predicted to be targeted by miR-26. Luciferase reporter assays were performed to confirm miR-26 regulation of the 3' UTR of target genes. The levels of miR-26 target genes (CHD1, GREB1 and KPNA2) were evaluated by western blotting and immunohistochemistry.
resultsEstrogen reduced the expression of miR-26a and miR-26b in ER+ breast cancer cells. Forced expression of miR-26a or miR-26b significantly inhibited the estrogen stimulated growth of ER+ breast cancer cells and tumor growth in xenograft models, whereas miR-26a/b depletion increased the growth of ER+ breast cancer cells in the absence of estrogen treatment. Screening of estrogen responsive genes, which were also predicted to be targeted by miR-26, identified GREB1 and nine other genes (AGPAT5, AMMECR1, CHD1, ERLIN1, HSPA8, KPNA2, MREG, NARG1, and PLOD2). Further verification has identified nine genes (AGPAT5, CHD1, ERLIN1, GREB1, HSPA8, KPNA2, MREG, NARG1 and PLOD2) which were directly targeted by miR-26 via their 3' UTR. Functional screening suggested only three estrogen regulated miR-26 target genes (CHD1, GREB1 and KPNA2) were involved in the regulation of estrogen promoted cell proliferation. Depletion of either CHD1, GREB1 or KPNA2 significantly abrogated the enhanced growth of ER+ breast cancer cells due to miR-26 depletion. We further demonstrated that estrogen stimulated c-MYC expression was both sufficient and necessary for the diminished expression of miR-26a and miR-26b.
conclusionsWe have identified a novel estrogen/MYC/miR-26 axis that mediates estrogen stimulated cell growth via CHD1, GREB1 and KPNA2.
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