ArticleMolecular cancer2018
MiR-25-3p promotes the proliferation of triple negative breast cancer by targeting BTG2.
Article in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 174 citations in OpenAlex.
- Circulating Cell-Free miR-25-3p Is Upregulated in Brazilian Patients with Prostate Cancer and Contributes to Tumor Aggressiveness.Non-coding RNA · 2026Article
- B-vitamin-associated miRNAs are enriched in pathways related to cell proliferation - insights from the general population.Nutrition & metabolism · 2026Article
- Hsa-miR-25-3p Inhibition Sensitizes Patient-Derived Glioblastoma Cells to Temozolomide via β-catenin Downregulation.Cellular and molecular neurobiology · 2026Article
- Article
- Integrative transcriptomic and machine learning framework reveals candidate genes and potential mechanisms of aflatoxin B1 exposure in breast cancer.Scientific reports · 2026Article
- Identification of novel exosomal miRNAs and their role in diagnosis and prognosis of triple negative breast cancer.BMC cancer · 2026Article
- Non-coding RNAs, a double-edged sword in breast cancer prognosis.Cancer cell international · 2025Review
- MiR-25-3p regulates pulmonary arteriovenous malformation after Glenn procedure in patients with univentricular heart via the PHLPP2-HIF-1α axis.Scientific reports · 2025Article
- MicroRNAs in breast cancer-new frontiers in diagnosis, targeted therapy, and prognosis assessment.Frontiers in oncology · 2025Review
- Association among Noncoding-RNAs, APRO Family Proteins, and Gut Microbiota in the Development of Breast Cancer.Oncology research · 2025Review
- Downregulation ofJournal of clinical medicine research · 2024Article
- Identification of somatic mutation-driven enhancers and their clinical utility in breast cancer.iScience · 2024Article
- CVD phenotyping in oncologic disorders: cardio-miRNAs as a potential target to improve individual outcomes in revers cardio-oncology.Journal of translational medicine · 2024Review
- AURKAIP1 actuates tumor progression through stabilizing DDX5 in triple negative breast cancer.Cell death & disease · 2023Article
- Serum miR-181а and miR-25 Levels in Patients with Breast Cancer or Benign Breast Disease.Doklady. Biochemistry and biophysics · 2023Article
- ER Negative Breast Cancer and miRNA: There Is More to Decipher Than What the Pathologist Can See!Biomedicines · 2023Review
- MicroRNA expression profiles associated with the metastatic ability of MDA‑MB‑231 breast cancer cells.Oncology letters · 2023Article
- Unraveling Therapeutic Opportunities and the Diagnostic Potential of microRNAs for Human Lung Cancer.Pharmaceutics · 2023Review
- miRNA-seq identification and clinical validation of CD138+ and circulating miR-25 in treatment response of multiple myeloma.Journal of translational medicine · 2023Article
- An Overview of Circulating Cell-Free Nucleic Acids in Diagnosis and Prognosis of Triple-Negative Breast Cancer.International journal of molecular sciences · 2023Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundTriple-negative breast cancer (TNBC) is highly invasive and aggressive and lacks specific molecular targets to improve the prognosis. MiR-25-3p promotes proliferation of many tumors and its role and underlying mechanisms in TNBC remain to be well elucidated.
methodsDifferential expression of miR-25-3p in TNBC was measured with quantitative real-time PCR (qRT-PCR) in both TNBC tissues and cell lines and was validated in the Cancer Genome Atlas (TCGA) database. The effects of miR-25-3p on proliferation, apoptosis capacity of TNBC were evaluated using Cell counting kit-8 (CCK-8), colony formation assay and Annexin V-FITC/PI analyses. The tumor growth in vivo was observed in xenograft model. Luciferase reporter assay, qPCR and western blot were performed to validate a potential target of miR-25-3p in TNBC. Involvement of the AKT and MAPK pathways was investigated by western blot.
resultsMiR-25-3p was found to be upregulated in TNBC in tissues and cell lines. MiR-25-3p promoted TNBC cell proliferation in vitro and tumor growth in xenograft model, while suppression of miR-25-3p induced cell apoptosis. The luciferase reporter assay confirmed that B-cell translocation gene 2 (BTG2) might be a direct target of miR-25-3p, and its expression was negatively regulated by miR-25-3p. Moreover, inhibition of BTG2 expression accounted for the role of miR-25-3p in TNBC. Furthermore, BTG2 suppression might indirectly activate the AKT and ERK-MAPK signaling pathways to mediate the downstream effects of miR-25-3p.
conclusionsThis study demonstrates that miR-25-3p promotes proliferation by targeting tumor suppressor BTG2 and may identify new diagnostic and therapeutic targets in TNBC.
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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.