ArticleAmerican journal of translational research2015
MiRNA-155 mediates TAM resistance by modulating SOCS6-STAT3 signalling pathway in breast cancer.
Article in American journal of translational research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 3 of them syntheses that pooled it.
What it found
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The trial behind it
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Who cites it
55 citing papers in PubMed, 3 syntheses or guidelines pooled it, 98 citations in OpenAlex.
- Hormone, Targeted, and Combinational Therapies for Breast Cancers: From Humans to Dogs.International journal of molecular sciences · 2024Pooled it
- MicroRNA Dysregulation in Early Breast Cancer Diagnosis: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2023Pooled it
- Pooled it
- Non-coding RNA-mediated mechanisms underlying tamoxifen resistance in breast cancer.Discover oncology · 2026Review
- Article
- Macrophage-cancer cell crosstalk in breast cancer chemotherapy resistance.Medical oncology (Northwood, London, England) · 2025Review
- Cold atmospheric plasma restores fulvestrant sensitivity by inhibiting CCND3 in the drug-resistant breast cancer cells.Scientific reports · 2025Article
- MicroRNA Landscape in Hepatocellular Carcinoma: Metabolic Re-Wiring, Predictive and Diagnostic Biomarkers, and Emerging Therapeutic Targets.Biomedicines · 2025Review
- miRNA-dependent resistance mechanisms to anti-hormonal therapies in estrogen receptor-positive breast cancer patients.Molecular therapy. Oncology · 2025Review
- Soy Isoflavone Genistein Enhances Tamoxifen Sensitivity in Breast Cancer via microRNA and Glucose Metabolism Modulation.International journal of molecular sciences · 2025Article
- Protective Effects of GalNac-Modified Red Blood Cell-Derived Extracellular Vesicles Against Liver Diseases.International journal of nanomedicine · 2025Article
- MiR-363-3p induces tamoxifen resistance in breast cancer cells through PTEN modulation.Scientific reports · 2024Article
- Extracellular vesicles as tools and targets in therapy for diseases.Signal transduction and targeted therapy · 2024Review
- Decoding the Promise and Challenges of miRNA-Based Cancer Therapies: An Essential Update on miR-21, miR-34, and miR-155.International journal of medical sciences · 2024Review
- Exosomal microRNAs in breast cancer: towards theranostic applications.Frontiers in molecular biosciences · 2024Review
- Therapeutic inhibition of miR-155 attenuates liver fibrosis via STAT3 signaling.Molecular therapy. Nucleic acids · 2023Article
- Non-Coding RNAs Modulating Estrogen Signaling and Response to Endocrine Therapy in Breast Cancer.Cancers · 2023Review
- The landscape of exosomal non-coding RNAs in breast cancer drug resistance, focusing on underlying molecular mechanisms.Frontiers in pharmacology · 2023Review
- A Single Variant in Pri-miRNA-155 Associated with Susceptibility to Hereditary Breast Cancer Promotes Aggressiveness in Breast Cancer Cells.International journal of molecular sciences · 2022Article
- MicroRNAs and JAK/STAT3 signaling: A new promising therapeutic axis in blood cancers.Genes & diseases · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is the second leading cause of cancer induced death in women. Tamoxifen is an endocrine therapy which is administered to 70% of all breast cancer patients with estrogen receptor alpha (ERα) expression. Despite the initial response, most patients eventually acquire resistance to the drug. MicroRNAs (miRNAs) are a class of small non-coding RNAs which have the ability to post-transcriptionally regulate gene expression. Although the role of a few miRNAs has been described in tamoxifen resistance, little is known about how concerted actions of miRNAs targeting biological networks contribute to its resistance. In this study, we identified that miR-155 is frequently up-regulated in breast cancer with tamoxifen resistance. Ectopic expression of miR-155 induces cell survival and resistance to TAM, whereas inhibition of miR-155 causes cells to apoptosis and enhances TAM sensitivity. Further, we identified SOCS6 as a new direct target of miR-155. Sustained overexpression of miR-155 resulted in repression of SOCS6 protein and mRNA levels, and knockdown of miR-155 increased SOCS6 expression. Introduction of SOCS6 cDNA lacking the 3'-UTR abrogated miR-155-induced cell survival and chemoresistance. Finally, it was verified that SOCS6 or inhibition of STAT3 could inhibit miR-155 STAT3 activation and cell proliferation. In conclusion, our study reveals a molecular link between miR-155 and SOCS6-STAT3 and presents an evidence that miR-155 is a critical therapeutic target in breast cancer.
Indexed as
Identifiers
26692956PMC4656789W2221944044What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.