ArticleOncotarget2016
The miR-644a/CTBP1/p53 axis suppresses drug resistance by simultaneous inhibition of cell survival and epithelial-mesenchymal transition in breast cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The trial behind it
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Who cites it
36 citing papers in PubMed, 59 citations in OpenAlex.
- Delineating theInternational journal of molecular sciences · 2026Review
- Tumor Suppressor p53 and MicroRNAs Interaction in Breast Cancer.Oncology research · 2026Review
- NAD(H)-dependent corepressor CTBP1 integrates metabolic signals to drive oncogenic programs.Frontiers in immunology · 2026Review
- Development and validation of a machine learning-driven mitochondrial gene signature for the diagnosis of breast cancer.Frontiers in immunology · 2025Article
- Role of EMT in drug resistance of breast cancer: molecular mechanisms and therapeutic strategies.Frontiers in oncology · 2025Review
- A highly potent bi-thiazole inhibitor of LOX rewires collagen architecture and enhances chemoresponse in triple-negative breast cancer.Cell chemical biology · 2024Article
- Discovery of novel microRNA mimic repressors of ribosome biogenesis.Nucleic acids research · 2024Article
- HMGA2 promotes cancer metastasis by regulating epithelial-mesenchymal transition.Frontiers in oncology · 2024Review
- Diagnostic applications and therapeutic option of Cascade CRISPR/Cas in the modulation of miRNA in diverse cancers: promises and obstacles.Journal of cancer research and clinical oncology · 2023Review
- Review
- LncRNA BCAR4 promotes migration, invasion, and chemo-resistance by inhibiting miR-644a in breast cancer.Journal of experimental & clinical cancer research : CR · 2023Article
- miR-489 Confines Uncontrolled Estrogen Signaling through a Negative Feedback Mechanism and Regulates Tamoxifen Resistance in Breast Cancer.International journal of molecular sciences · 2022Article
- Targeting HIF1-alpha/miR-326/ITGA5 axis potentiates chemotherapy response in triple-negative breast cancer.Breast cancer research and treatment · 2022Article
- CRISPR/Cas9Iranian journal of public health · 2022Article
- Sumoylation of Cas9 at lysine 848 regulates protein stability and DNA binding.Life science alliance · 2022Article
- Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial-Mesenchymal Plasticity.Cancers · 2021Review
- Transcriptional Analyses of Acute Exposure to Methylmercury on Erythrocytes of Loggerhead Sea Turtle.Toxics · 2021Article
- Effective tools for RNA-derived therapeutics: siRNA interference or miRNA mimicry.Theranostics · 2021Review
- A circGLIS3/miR-644a/PTBP1 positive feedback loop promotes the malignant biological progressions of non-small cell lung cancer.American journal of cancer research · 2021Article
- Epithelial-Mesenchymal Transition Programs and Cancer Stem Cell Phenotypes: Mediators of Breast Cancer Therapy Resistance.Molecular cancer research : MCR · 2020Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor cells develop drug resistance which leads to recurrence and distant metastasis. MicroRNAs are key regulators of tumor pathogenesis; however, little is known whether they can sensitize cells and block metastasis simultaneously. Here, we report miR-644a as a novel inhibitor of both cell survival and EMT whereby acting as pleiotropic therapy-sensitizer in breast cancer. We showed that both miR-644a expression and its gene signature are associated with tumor progression and distant metastasis-free survival. Mechanistically, miR-644a directly targets the transcriptional co-repressor C-Terminal Binding Protein 1 (CTBP1) whose knock-outs by the CRISPR-Cas9 system inhibit tumor growth, metastasis, and drug resistance, mimicking the phenotypes induced by miR-644a. Furthermore, downregulation of CTBP1 by miR-644a upregulates wild type- or mutant-p53 which acts as a 'molecular switch' between G1-arrest and apoptosis by inducing cyclin-dependent kinase inhibitor 1 (p21, CDKN1A, CIP1) or pro-apoptotic phorbol-12-myristate-13-acetate-induced protein 1 (Noxa, PMAIP1), respectively. Interestingly, an increase in mutant-p53 by either overexpression of miR-644a or downregulation of CTBP1 was enough to shift this balance in favor of apoptosis through upregulation of Noxa. Notably, p53-mutant patients, but not p53-wild type ones, with high CTBP1 have a shorter survival suggesting that CTBP1 could be a potential prognostic factor for breast cancer patients with p53 mutations. Overall, re-activation of the miR-644a/CTBP1/p53 axis may represent a new strategy for overcoming both therapy resistance and metastasis.
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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.