ArticleOncogene2013
BTG2 loss and miR-21 upregulation contribute to prostate cell transformation by inducing luminal markers expression and epithelial-mesenchymal transition.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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.
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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
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.
- Global research landscape and emerging trends of non-coding RNAs in prostate cancer: a bibliometric analysis.Frontiers in pharmacology · 2024Pooled it
- The regulatory role of KIAA1429 in epithelial-mesenchymal transition in cervical cancer via mediating m6A modification of BTG2.Cytotechnology · 2025Article
- CRISPR/Cas9 Technology Providing the Therapeutic Landscape of Metastatic Prostate Cancer.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Role of MicroRNA-21 in Prostate Cancer Progression and Metastasis: Molecular Mechanisms to Therapeutic Targets.Annals of surgical oncology · 2024Review
- Prognostic effect of DNA methylation ofHeliyon · 2024Article
- MicroRNA-21 in urologic cancers: from molecular mechanisms to clinical implications.Frontiers in cell and developmental biology · 2024Review
- Btg2 Promotes Focal Segmental Glomerulosclerosis via Smad3-Dependent Podocyte-Mesenchymal Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The Effect of Gene Editing by CRISPR-Cas9 of miR-21 and the Indirect Target MMP9 in Metastatic Prostate Cancer.International journal of molecular sciences · 2023Article
- Unraveling Therapeutic Opportunities and the Diagnostic Potential of microRNAs for Human Lung Cancer.Pharmaceutics · 2023Review
- Article
- BTG2 as a tumor target for the treatment of luminal A breast cancer.Experimental and therapeutic medicine · 2022Article
- Article
- Semen as a rich source of diagnostic biomarkers for prostate cancer: latest evidence and implications.Molecular and cellular biochemistry · 2022Review
- Expression and methylation status ofGastroenterology and hepatology from bed to bench · 2022Article
- B-Cell Translocation Gene 2 Upregulation Is Associated with Favorable Prognosis in Lung Adenocarcinoma and Prolonged Patient Survival.Journal of oncology · 2022Article
- Article
- Ribonucleic acid-binding protein CPSF6 promotes glycolysis and suppresses apoptosis in hepatocellular carcinoma cells by inhibiting the BTG2 expression.Biomedical engineering online · 2021Article
- Micro1278 Leads to Tumor Growth Arrest, Enhanced Sensitivity to Oxaliplatin and Vitamin D and Inhibits MetastasisFrontiers in oncology · 2021Article
- Requirement for LIM kinases in acute myeloid leukemia.Leukemia · 2020Article
- Role of specialized composition of SWI/SNF complexes in prostate cancer lineage plasticity.Nature communications · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer is one of the leading causes of cancer-related death in men. Despite significant advances in prostate cancer diagnosis and management, the molecular events involved in the transformation of normal prostate cells into cancer cells have not been fully understood. It is generally accepted that prostate cancer derives from the basal compartment while expressing luminal markers. We investigated whether downregulation of the basal protein B-cell translocation gene 2 (BTG2) is implicated in prostate cancer transformation and progression. Here we show that BTG2 loss can shift normal prostate basal cells towards luminal markers expression, a phenotype also accompanied by the appearance of epithelial-mesenchymal transition (EMT) traits. We also show that the overexpression of microRNA (miR)-21 suppresses BTG2 levels and promotes the acquisition of luminal markers and EMT in prostate cells. Furthermore, by using an innovative lentiviral vector able to compete with endogenous mRNA through the overexpression of the 3'-untranslated region of BTG2, we demonstrate that in prostate tumor cells, the levels of luminal and EMT markers can be reduced by derepression of BTG2 from microRNA-mediated control. Finally, we show that the loss of BTG2 expression confers to non-tumorigenic prostate cells ability to grow in an orthotopic murine model, thus demonstrating the central role of BTG2 downregulaton in prostate cancer biology.
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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.