ArticleOncotarget2015
Combined inhibition of EGFR and c-ABL suppresses the growth of triple-negative breast cancer growth through inhibition of HOTAIR.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 71 citations in OpenAlex.
- Long Intergenic Non-Coding RNAs andNon-coding RNA · 2025Review
- Design, synthesis, molecular docking, andSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Article
- Boolean modeling of breast cancer signaling pathways uncovers mechanisms of drug synergy.PloS one · 2024Article
- Exploiting Long Non-Coding RNAs and Circular RNAs as Pharmacological Targets in Triple-Negative Breast Cancer Treatment.Cancers · 2023Review
- HOTAIR: a potential metastatic, drug-resistant and prognostic regulator of breast cancer.Molecular cancer · 2023Review
- Review
- Article
- Article
- Advances in Pathophysiology of Triple-Negative Breast Cancer: The Potential of lncRNAs for Clinical Diagnosis, Treatment, and Prognostic Monitoring.Molecular biotechnology · 2021Review
- Potentiating Therapeutic Effects of Epidermal Growth Factor Receptor Inhibition in Triple-Negative Breast Cancer.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Current Knowledge of Long Non-Coding RNA HOTAIR in Breast Cancer Progression and Its Application.Life (Basel, Switzerland) · 2021Review
- The long non-coding RNA landscape in triple-negative breast cancer.Cell proliferation · 2021Review
- Aptamer-guided targeting of the intracellular long-noncoding RNAAmerican journal of cancer research · 2021Article
- The role of HOTAIR/miR-152-3p/LIN28B in regulating the progression of endometrial squamous carcinoma.Archives of medical science : AMS · 2021Article
- Modulatory Role of microRNAs in Triple Negative Breast Cancer with Basal-Like Phenotype.Cancers · 2020Review
- Bioengineered siRNA-Based Nanoplatforms Targeting Molecular Signaling Pathways for the Treatment of Triple Negative Breast Cancer: Preclinical and Clinical Advancements.Pharmaceutics · 2020Review
- The emerging role of the long non-coding RNA HOTAIR in breast cancer development and treatment.Journal of translational medicine · 2020Review
- Long noncoding RNA HOTAIR promotes invasion of breast cancer cells through chondroitin sulfotransferase CHST15.International journal of cancer · 2019Article
- Long non-coding RNA DRHC inhibits the proliferation of cancer cells in triple negative breast cancer by downregulating long non-coding RNA HOTAIR.Oncology letters · 2019Article
- New Insights into the Implication of Epigenetic Alterations in the EMT of Triple Negative Breast Cancer.Cancers · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Triple-negative breast cancer (TNBC) does not express conventional therapeutic targets and is the only type of malignant breast cancer for which no designated FDA-approved targeted therapy is available. Although overexpression of epidermal growth factor receptor (EGFR) is frequently found in TNBC, the therapeutic effect of EGFR inhibitors in TNBC has been underwhelming. Here we show that co-treatment with clinically validated inhibitors of c-ABL (imatinib) and EGFR (lapatinib) results in synergistic growth inhibition in TNBC cells. The dual treatment leads to synergistic repression of the long non-coding RNA (lncRNA) HOTAIR (HOX Antisense Intergenic RNA). HOTAIR has been known to induce tumor growth and metastasis in breast cancer. Depleting HOTAIR alone phenocopies the dual treatment in growth suppression. We show that expression of HOTAIR is regulated by β-catenin through a LEF1/TCF4-binding site. The dual treatment blocks nuclear expression of β-catenin and prevents its recruitment to the HOTAIR promoter. Consistently, forced expression of β-catenin rescued HOTAIR expression and cell viability in the presence of both drugs. Upregulation of HOTAIR is associated with TNBC in cell lines and a cohort of primary tumors. This study elucidates a previously unidentified mechanism in TNBC linking signaling with lncRNA regulation which may be exploited for therapeutic gain.
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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.