ArticleOncogene2016
MiR-16 mediates trastuzumab and lapatinib response in ErbB-2-positive breast and gastric cancer via its novel targets CCNJ and FUBP1.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 54 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Pooled it
- Tumor microenvironment-driven microRNA dysregulation: Key interactions in colorectal cancer progression.World journal of gastrointestinal oncology · 2026Review
- Interplay Between MicroRNAs and Breast Cancer Therapies: Personalized Therapeutic Potential for HER2-Low Breast Cancer.Cancers · 2025Review
- Transcriptomic-Based Identification of miR-125a Novel Targets in Human Hepatocarcinoma Cells.Biomolecules · 2025Article
- FUBP1 in human cancer: Characteristics, functions, and potential applications.Translational oncology · 2024Review
- miRNAs as biomarkers of therapeutic response to HER2-targeted treatment in breast cancer: A systematic review.Biochemistry and biophysics reports · 2024Review
- RNA splicing alterations in lung cancer pathogenesis and therapy.Cancer pathogenesis and therapy · 2023Review
- Landscape of NcRNAs involved in drug resistance of breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Article
- Exosomal miRNAs as novel avenues for breast cancer treatment.Frontiers in genetics · 2023Review
- Breast cancer: miRNAs monitoring chemoresistance and systemic therapy.Frontiers in oncology · 2023Review
- Discovery of Anthranilic Acid Derivatives as Difluoromethylornithine Adjunct Agents That Inhibit Far Upstream Element Binding Protein 1 (FUBP1) Function.Journal of medicinal chemistry · 2022Article
- FBP1 knockdown decreases ovarian cancer formation and cisplatin resistance through EZH2-mediated H3K27me3.Bioscience reports · 2022Article
- MicroRNAs as a clue to overcome breast cancer treatment resistance.Cancer metastasis reviews · 2022Review
- Investigating the Active Substance and Mechanism of San-Jiu-Wei-Tai Granules via UPLC-QE-Orbitrap-MS and Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- An overview of resistance to Human epidermal growth factor receptor 2 (Her2) targeted therapies in breast cancer.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- miR-221 confers lapatinib resistance by negatively regulating p27Cancer science · 2021Article
- Breast Cancer Response to Therapy: Can microRNAs Lead the Way?Journal of mammary gland biology and neoplasia · 2021Review
- FUBP1 mediates the growth and metastasis through TGFβ/Smad signaling in pancreatic adenocarcinoma.International journal of molecular medicine · 2021Article
- Exosomal microRNAs: Pleiotropic Impacts on Breast Cancer Metastasis and Their Clinical Perspectives.Biology · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
19 authors at 9 institutions in 3 countries.
Funding
Abstract
ErbB-2 amplification/overexpression accounts for an aggressive breast cancer (BC) subtype (ErbB-2-positive). Enhanced ErbB-2 expression was also found in gastric cancer (GC) and has been correlated with poor clinical outcome. The ErbB-2-targeted therapies trastuzumab (TZ), a monoclonal antibody, and lapatinib, a tyrosine kinase inhibitor, have proved highly beneficial. However, resistance to such therapies remains a major clinical challenge. We here revealed a novel mechanism underlying the antiproliferative effects of both agents in ErbB-2-positive BC and GC. TZ and lapatinib ability to block extracellular signal-regulated kinases 1/2 and phosphatidylinositol-3 kinase (PI3K)/AKT in sensitive cells inhibits c-Myc activation, which results in upregulation of miR-16. Forced expression of miR-16 inhibited in vitro proliferation in BC and GC cells, both sensitive and resistant to TZ and lapatinib, as well as in a preclinical BC model resistant to these agents. This reveals miR-16 role as tumor suppressor in ErbB-2-positive BC and GC. Using genome-wide expression studies and miRNA target prediction algorithms, we identified cyclin J and far upstream element-binding protein 1 (FUBP1) as novel miR-16 targets, which mediate miR-16 antiproliferative effects. Supporting the clinical relevance of our results, we found that high levels of miR-16 and low or null FUBP1 expression correlate with TZ response in ErbB-2-positive primary BCs. These findings highlight a potential role of miR-16 and FUBP1 as biomarkers of sensitivity to TZ therapy. Furthermore, we revealed miR-16 as an innovative therapeutic agent for TZ- and lapatinib-resistant ErbB-2-positive BC and GC.
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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.