ArticleThe Journal of experimental medicine2004
Activation of PI3K is indispensable for interleukin 7-mediated viability, proliferation, glucose use, and growth of T cell acute lymphoblastic leukemia cells.
Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers.
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Who cites it
163 citing papers in PubMed, 273 citations in OpenAlex.
- The Oral PI3Kδ Inhibitor Linperlisib for the Treatment of Relapsed and/or Refractory Follicular Lymphoma: A Phase II, Single-Arm, Open-Label Clinical Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Trial
- B7 costimulation antagonizes RORγt+ regulatory T cells and immune tolerance in the intestine.The Journal of experimental medicine · 2026Article
- Cytokines, Signaling and Epigenetic Mechanisms: Shaping the Acute Lymphoblastic Leukemia Microenvironment.Cells · 2026Review
- Common gamma chain cytokines-driven optimization of chimeric antigen receptor T cells: Mechanistic insights and future directions.World journal of clinical oncology · 2026Review
- Decoding NOTCH1: From T-Cell Development Guardian to Driver of Pediatric T-Cell Lymphoblastic Lymphoma.International journal of molecular sciences · 2026Review
- Convergent Multistage Evidence Implicates the CCR2-Artemin Immune-Inflammation Axis in Acute Myeloid Leukemia.Mediators of inflammation · 2026Article
- Metabolic reprogramming by PRDM16 drives cytarabine resistance in acute myeloid leukemia.Haematologica · 2025Article
- Machine learning analysis reveals tumor heterogeneity and stromal-immune niches in breast cancer.NPJ digital medicine · 2025Article
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- Interleukin-7 promotes porcine early embryogenesis in vitro and inner cell mass development through PI3K/AKT pathway after parthenogenetic activation.Scientific reports · 2025Article
- Potential drug targets for asthma identified through mendelian randomization analysis.Respiratory research · 2025Article
- IL-7 promotes mRNA vaccine-induced long-term immunity.Journal of nanobiotechnology · 2024Article
- Rapamycin Prevents Expansion of Costimulation Blockade-resistant CD8+ Alloreactive Memory Cells following Depletional Induction in Renal Transplant Recipients.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Heat shock proteins as hallmarks of cancer: insights from molecular mechanisms to therapeutic strategies.Journal of hematology & oncology · 2024Review
- Metabolic dialogues: regulators of chimeric antigen receptor T cell function in the tumor microenvironment.Molecular oncology · 2024Review
- Inflammation as a driver of hematological malignancies.Frontiers in oncology · 2024Review
- Prognostic impact ofTherapeutic advances in hematology · 2024Article
- Amniotic MSC affect CD8 naive polarization toward SLEC/MPEC subsets by down-modulating IL-12Rβ1 and IL-2Rα signaling pathways.iScience · 2023Article
- Developing Targeted Therapies for T Cell Acute Lymphoblastic Leukemia/Lymphoma.Current hematologic malignancy reports · 2023Review
103 more citing papers are in PubMed but not listed here.
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Interleukin (IL)-7 is essential for normal T cell development. Previously, we have shown that IL-7 increases viability and proliferation of T cell acute lymphoblastic leukemia (T-ALL) cells by up-regulating Bcl-2 and down-regulating the cyclin-dependent kinase inhibitor p27kip1. Here, we examined the signaling pathways via which IL-7 mediates these effects. We investigated mitogen-activated protein kinase (MEK)-extracellular signal-regulated kinase (Erk) and phosphatidylinositol-3-kinase (PI3K)-Akt (protein kinase B) pathways, which have active roles in T cell expansion and have been implicated in tumorigenesis. IL-7 induced activation of the MEK-Erk pathway in T-ALL cells; however, inhibition of the MEK-Erk pathway by the use of the cell-permeable inhibitor PD98059, did not affect IL-7-mediated viability or cell cycle progression of leukemic cells. IL-7 induced PI3K-dependent phosphorylation of Akt and its downstream targets GSK-3, FOXO1, and FOXO3a. PI3K activation was mandatory for IL-7-mediated Bcl-2 up-regulation, p27kip1 down-regulation, Rb hyperphosphorylation, and consequent viability and cell cycle progression of T-ALL cells. PI3K signaling was also required for cell size increase, up-regulation of CD71, expression of the glucose transporter Glut1, uptake of glucose, and maintenance of mitochondrial integrity. Our results implicate PI3K as a major effector of IL-7-induced viability, metabolic activation, growth and proliferation of T-ALL cells, and suggest that PI3K and its downstream effectors may represent molecular targets for therapeutic intervention in T-ALL.
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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.