ArticleOncogene2017
DEPTOR is a direct NOTCH1 target that promotes cell proliferation and survival in T-cell leukemia.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Not only a therapeutic target; mTOR in Hodgkin lymphoma and acute lymphoblastic leukemia.Frontiers in oncology · 2024Pooled it
- An injectable nano-hydroxyapatite-incorporated hydrogel with sustained release of Notoginsenoside R1 enhances bone regeneration by promoting angiogenesis through Notch1/Akt signaling.Journal of advanced research · 2026Article
- Identification of ANXA1 as a Novel Upstream Negative Regulator of Notch1 Function in AML.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- PUM1 Promotes Tumor Progression by Activating DEPTOR-Meditated Glycolysis in Gastric Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The UBE2C/CDH1/DEPTOR axis is an oncogene and tumor suppressor cascade in lung cancer cells.The Journal of clinical investigation · 2023Article
- Effects of polymer carriers on the occurrence and development of autophagy in drug delivery.Nanoscale advances · 2022Review
- Inhibition of mitochondrial complex I reverses NOTCH1-driven metabolic reprogramming in T-cell acute lymphoblastic leukemia.Nature communications · 2022Article
- Article
- Bipartite binding and partial inhibition links DEPTOR and mTOR in a mutually antagonistic embrace.eLife · 2021Article
- WEE1 inhibition induces glutamine addiction in T-cell acute lymphoblastic leukemia.Haematologica · 2021Article
- Nuclear ErbB2 represses DEPTOR transcription to inhibit autophagy in breast cancer cells.Cell death & disease · 2021Article
- [The role and research progress of NOTCH1 in T-cell acute lymphoblastic leukemia].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2021Article
- Regulatory role of DEPTOR‑mediated cellular autophagy and mitochondrial reactive oxygen species in angiogenesis in multiple myeloma.International journal of molecular medicine · 2021Article
- DNA Methylation in T-Cell Acute Lymphoblastic Leukemia: In Search for Clinical and Biological Meaning.International journal of molecular sciences · 2021Review
- Review
- DEPTOR stabilizes ErbB2 to promote the proliferation and survival of ErbB2-positive breast cancer cells.Theranostics · 2021Article
- Genome-Wide Analysis IdentifiesFrontiers in cell and developmental biology · 2021Article
- DEPTOR is a direct p53 target that suppresses cell growth and chemosensitivity.Cell death & disease · 2020Article
- DNA methylation-based classification reveals difference between pediatric T-cell acute lymphoblastic leukemia and normal thymocytes.Leukemia · 2020Article
- Direct Phosphorylation and Stabilization of MYC by Aurora B Kinase Promote T-cell Leukemogenesis.Cancer cell · 2020Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant activation of NOTCH1 signaling plays a vital role in the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL). Yet the molecular events downstream of NOTCH1 that drive T-cell leukemogenesis remain incompletely understood. Starting from genome-wide gene-expression profiling to seek important NOTCH1 transcriptional targets, we identified DEP-domain containing mTOR-interacting protein (DEPTOR), which was previously shown to be important in multiple myeloma but remains functionally unclear in other hematological malignancies. Mechanistically, we demonstrated NOTCH1 directly bound to and activated the human DEPTOR promoter in T-ALL cells. DEPTOR depletion abolished cellular proliferation, attenuated glycolytic metabolism and enhanced cell death, while ectopically expressed DEPTOR significantly promoted cell growth and glycolysis. We further showed that DEPTOR depletion inhibited while its overexpression enhanced AKT activation in T-ALL cells. Importantly, AKT inhibition completely abrogated DEPTOR-mediated cell growth advantages. Moreover, DEPTOR depletion in a human T-ALL xenograft model significantly delayed T-ALL onset and caused a substantial decrease of AKT activation in leukemic blasts. We thus reveal a novel mechanism involved in NOTCH1-driven leukemogenesis, identifying the transcriptional control of DEPTOR and its regulation of AKT as additional key elements of the leukemogenic program activated by NOTCH1.
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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.