ArticleLeukemia2017
Regulation of PI3K signaling in T-cell acute lymphoblastic leukemia: a novel PTEN/Ikaros/miR-26b mechanism reveals a critical targetable role for PIK3CD.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 62 citations in OpenAlex.
- TET1 deficiency amplifies macrophage inflammatory signaling associated with Crohn's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Carbon dot-based treatment for bacterial pneumonia by promoting a PI3K-mediated M1 polarization of macrophages.Journal of nanobiotechnology · 2025Article
- Unveiling the omics tapestry of B-acute lymphoblastic leukemia: bridging genomics, metabolomics, and immunomics.Scientific reports · 2025Article
- MiR-363-3p induces tamoxifen resistance in breast cancer cells through PTEN modulation.Scientific reports · 2024Article
- Immune checkpoints and ncRNAs: pioneering immunotherapy approaches for hematological malignancies.Cancer cell international · 2024Review
- Leveraging altered lipid metabolism in treating B cell malignancies.Progress in lipid research · 2024Review
- RNA-seq-based miRNA signature as an independent predictor of relapse in pediatric B-cell acute lymphoblastic leukemia.Blood advances · 2024Article
- JAK3/STAT5 signaling-triggered upregulation of PIK3CD contributes to gastric carcinoma development.Journal of cell communication and signaling · 2024Article
- Evaluation of MicroRNA as Minimal Residual Disease in Leukemia: Diagnostic and Prognostic Approach: A Review.Iranian journal of public health · 2023Review
- The Promising Role of Non-Coding RNAs as Biomarkers and Therapeutic Targets for Leukemia.Genes · 2023Review
- Silencing of IRF8 Mediated by m6A Modification Promotes the Progression of T-Cell Acute Lymphoblastic Leukemia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- miRNA Pattern in Hypoxic Microenvironment of Kidney Cancer-Role of PTEN.Biomolecules · 2022Article
- Article
- MicroRNAs as Modulators of the Immune Response in T-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2022Review
- PI3K Targeting in Non-solid Cancer.Current topics in microbiology and immunology · 2022Review
- Polyphenols: Chemoprevention and therapeutic potentials in hematological malignancies.Frontiers in nutrition · 2022Review
- A Review of Phosphocreatine 3 Kinase δ Subtype (PI3Kδ) and Its Inhibitors in Malignancy.Medical science monitor : international medical journal of experimental and clinical research · 2021Review
- T-ALL can evolve to oncogene independence.Leukemia · 2021Article
- Tumor-suppressive microRNA-551b-3p targets H6PD to inhibit gallbladder cancer progression.Cancer gene therapy · 2021Article
- MicroRNA as a Prognostic and Diagnostic Marker in T-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
23 authors at 6 institutions in 3 countries.
Funding
Abstract
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy, and T-ALL patients are prone to early disease relapse and suffer from poor outcomes. The PTEN, PI3K/AKT and Notch pathways are frequently altered in T-ALL. PTEN is a tumor suppressor that inactivates the PI3K pathway. We profiled miRNAs in Pten-deficient mouse T-ALL and identified miR-26b as a potentially dysregulated gene. We validated decreased expression levels of miR-26b in mouse and human T-ALL cells. In addition, expression of exogenous miR-26b reduced proliferation and promoted apoptosis of T-ALL cells in vitro, and hindered progression of T-ALL in vivo. Furthermore, miR-26b inhibited the PI3K/AKT pathway by directly targeting PIK3CD, the gene encoding PI3Kδ, in human T-ALL cell lines. ShRNA for PIK3CD and CAL-101, a PIK3CD inhibitor, reduced the growth and increased apoptosis of T-ALL cells. Finally, we showed that PTEN induced miR-26b expression by regulating the differential expression of Ikaros isoforms that are transcriptional regulators of miR-26b. These results suggest that miR-26b functions as a tumor suppressor in the development of T-ALL. Further characterization of targets and regulators of miR-26b may be promising for the development of novel therapies.
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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.