ArticleScientific reports2015
MiR-129-3p promotes docetaxel resistance of breast cancer cells via CP110 inhibition.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- MicroRNA-129-3p Suppresses Tumor Progression and Chemoradioresistance in Head and Neck Squamous Cell Carcinoma.Current oncology (Toronto, Ont.) · 2025Article
- Identification of chemoresistance associated key genes-miRNAs-TFs in docetaxel resistant breast cancer by bioinformatics analysis.3 Biotech · 2024Article
- The regulation of microRNAs on chemoresistance in triple-negative breast cancer: a recent update.Epigenomics · 2024Review
- Identification of miRNAs that target Fcγ receptor-mediated phagocytosis during macrophage activation syndrome.Frontiers in immunology · 2024Article
- lncRNA XIST/miR‑129‑2‑3p axis targets CCP110 to regulate the proliferation, invasion and migration of endometrial cancer cells.Experimental and therapeutic medicine · 2023Article
- Breast cancer: miRNAs monitoring chemoresistance and systemic therapy.Frontiers in oncology · 2023Review
- Docetaxel suppressed cell proliferation through Smad3/HIF-1α-mediated glycolysis in prostate cancer cells.Cell communication and signaling : CCS · 2022Article
- Circular RNA coiled-coil domain containing 66 regulates malignant development of papillary thyroid carcinoma by upregulating La ribonucleoprotein 1Bioengineered · 2022Article
- MicroRNA Alterations Induced in Human Skin by Diesel Fumes, Ozone, and UV Radiation.Journal of personalized medicine · 2022Article
- LncRNA TTN-AS1 confers tamoxifen resistance in breast cancer via sponging miR-107 to modulate PI3K/AKT signaling pathway.American journal of translational research · 2022Article
- microRNA-4429-5p suppresses the malignant development of colon cancer by targeting matrix metalloproteinase 16.In vitro cellular & developmental biology. Animal · 2021Article
- Breast Cancer Response to Therapy: Can microRNAs Lead the Way?Journal of mammary gland biology and neoplasia · 2021Review
- miR-129-3p Targeting of MCU Protects Against Glucose Fluctuation-Mediated Neuronal Damage via a Mitochondrial-Dependent Intrinsic Apoptotic Pathway.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- The Role of Non-Coding RNAs in Breast Cancer Drug Resistance.Frontiers in oncology · 2021Review
- Contribution of miRNAs in the Pathogenesis of Breast Cancer.Frontiers in oncology · 2021Review
- miR-129-3p alleviates chondrocyte apoptosis in knee joint fracture-induced osteoarthritis through CPEB1.Journal of orthopaedic surgery and research · 2020Article
- Connecting the Missing Dots: ncRNAs as Critical Regulators of Therapeutic Susceptibility in Breast Cancer.Cancers · 2020Review
- Non-Coding RNAs as Regulators and Markers for Targeting of Breast Cancer and Cancer Stem Cells.Cancers · 2020Review
- MiR-129-5p promotes docetaxel resistance in prostate cancer by down-regulating CAMK2N1 expression.Journal of cellular and molecular medicine · 2020Article
- RILPL2 regulates breast cancer proliferation, metastasis, and chemoresistance via the TUBB3/PTEN pathway.American journal of cancer research · 2019Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Docetaxel is commonly used as an effective chemotherapeutic agent in breast cancer treatment, but the underlying mechanisms of drug resistance are not fully understood. The purpose of this study was to investigate the possible role of miR-129-3p in breast cancer cell resistance to docetaxel. MiR-129 and miR-129-3p inhibitor were transfected into breast cancer cells to investigate their effects on chemoresistance to docetaxel. The function of miR-129-3p was evaluated by apoptosis, cell proliferation, and cell cycle assays. We found that miR-129-3p was up-regulated in MDA-MB-231/Doc cells, concurrent with CP110 down-regulation, compared to the parental MDA-MB-231 cells. In vitro drug sensitivity assays demonstrated that miR-129-3p inhibition sensitized MDA-MB-231/Doc and MCF-7 cells to docetaxel, whereas miR-129 overexpression enhanced MDA-MB-231 and MCF-7 cell resistance to docetaxel. Ectopic miR-129 expression reduced CP110 expression and the luciferase activity of a CP110 3' untranslated region-based reporter construct in MDA-MB-231 cells, suggesting that CP110 is a direct miR-129-3p target. We demonstrated that restoration of CP110 expression in MDA-MB-231 and MCF-7 cells by miR-129 overexpression rendered the cells sensitive to docetaxel. In a nude xenograft model, miR-129 up-regulation significantly decreased MDA-MB-231 cells' response to docetaxel. Our findings suggest that miR-129-3p down-regulation potentially sensitizes breast cancer cells to docetaxel treatment.
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Registered trials
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