ArticleScientific reports2022
PTEN/PI3K/Akt pathway alters sensitivity of T-cell acute lymphoblastic leukemia to L-asparaginase.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Synergistic apoptotic induction in acute lymphoblastic leukemia cells: exploring the role of EAAT1 inhibition by UCPH-101 in combination with asparaginase.Molecular biology reports · 2026Article
- The Role of miRNA-21 in the Metastasis of Hepatocellular Carcinoma as a Therapeutic Target.International journal of hematology-oncology and stem cell research · 2026Review
- Neferine inhibits vascular smooth muscle cell proliferation and migration in atherosclerosis by targeting CYS130 and PHE252 in PTEN.Frontiers in pharmacology · 2026Article
- SERPINA1 gene regulates the tumorigenesis and progression of breast cancer through PI3K/AKT signaling pathway and tumor immune microenvironment.Scientific reports · 2025Article
- Review
- Multifaceted Cooperation Between WNT and PI3K Signaling Axis through the Long Noncoding RNA SNHG16 and TCF7 in de novo Acute Lymphoblastic Leukemia Patients.Iranian biomedical journal · 2025Article
- A metabolic synthetic lethality of phosphoinositide 3-kinase-driven cancer.Nature communications · 2025Article
- The Role of MicroRNAs, CircRNAs, and LncRNAs in Chronic Lymphocytic Leukemia.Current pharmaceutical design · 2025Review
- The Role of PTEN in Chemoresistance Mediated by the HIF-1α/YY1 Axis in Pediatric Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2024Article
- Development of combination therapies with BTK inhibitors and dasatinib to treat CNS-infiltrating E2A-PBX1+/preBCR+ ALL.Blood advances · 2024Article
- Knockdown of miR-24 Suppressed the Tumor Growth of Cervical Carcinoma Through Regulating PTEN/PI3K/AKT Signaling Pathway.Biochemical genetics · 2024Article
- Suppression of malignant melanoma by knocking down growth differentiation factor-15 via inhibiting PTEN/PI3K/AKT signaling pathway.Journal of Cancer · 2024Article
- Effect of 5-Aza-2'-deoxycytidine on T-cell acute lymphoblastic leukemia cell biological behaviors and PTEN expression.CytoJournal · 2024Article
- YBX1 as an oncogenic factor in T-cell acute lymphoblastic leukemia.Blood advances · 2023Article
- Vasoactive intestinal peptide exerts therapeutic action by regulating PTEN in a model of Sjögren's disease.Immunity, inflammation and disease · 2023Article
- Possible mechanism of metabolic and drug resistance with L-asparaginase therapy in childhood leukaemia.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Childhood T-cell acute lymphoblastic leukemia (T-ALL) still remains a therapeutic challenge due to relapses which are resistant to further treatment. L-asparaginase (ASNase) is a key therapy component in pediatric T-ALL and lower sensitivity of leukemia cells to this drug negatively influences overall treatment efficacy and outcome. PTEN protein deletion and/or activation of the PI3K/Akt signaling pathway leading to altered cell growth and metabolism are emerging as a common feature in T-ALL. We herein investigated the relationship amongst PTEN deletion, ASNase sensitivity and glucose metabolism in T-ALL cells. First, we found significant differences in the sensitivity to ASNase amongst T-ALL cell lines. While cell lines more sensitive to ASNase were PTEN wild type (WT) and had no detectable level of phosphorylated Akt (P-Akt), cell lines less sensitive to ASNase were PTEN-null with high P-Akt levels. Pharmacological inhibition of Akt in the PTEN-null cells rendered them more sensitive to ASNase and lowered their glycolytic function which then resembled PTEN WT cells. In primary T-ALL cells, although P-Akt level was not dependent exclusively on PTEN expression, their sensitivity to ASNase could also be increased by pharmacological inhibition of Akt. In summary, we highlight a promising therapeutic option for T-ALL patients with aberrant PTEN/PI3K/Akt signaling.
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