ArticleOncotarget2016
The NEDD8-activating enzyme inhibitor MLN4924 induces G2 arrest and apoptosis in T-cell acute lymphoblastic leukemia.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- MYC-induced USP10 stabilizes SOX4 to promote thymocyte proliferation and leukemia onset in mice.Nature communications · 2026Article
- Pharmacological inhibition of host cell neddylation reduces intoxication of cells by diphtheria toxin and clostridial enterotoxins TcdB and C2.Microbiology spectrum · 2026Article
- A scalable reinforcement learning approach for screening large peptide libraries for bioactive peptide discovery.Nature communications · 2025Article
- SUMOylation of the lysine-less tumor suppressor p14ARF counters ubiquitylation-dependent degradation.Cell death & disease · 2025Article
- Therapeutic targeting of the NOTCH1 and neddylation pathways in T cell acute lymphoblastic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Protein neddylation and its role in health and diseases.Signal transduction and targeted therapy · 2024Review
- Article
- The Next Frontier: Translational Development of Ubiquitination, SUMOylation, and NEDDylation in Cancer.International journal of molecular sciences · 2022Review
- Emerging role of protein modification in inflammatory bowel disease.Journal of Zhejiang University. Science. B · 2022Review
- Circadian rhythms and cancers: the intrinsic links and therapeutic potentials.Journal of hematology & oncology · 2022Review
- Advances in Cancer Treatment by Targeting the Neddylation Pathway.Frontiers in cell and developmental biology · 2021Review
- T-cell Acute Lymphoblastic Leukemia: A Roadmap to Targeted Therapies.Blood cancer discovery · 2021Review
- HucMSC-exosomes carrying miR-326 inhibit neddylation to relieve inflammatory bowel disease in mice.Clinical and translational medicine · 2020Article
- Ubiquitin and ubiquitin-like molecules in DNA double strand break repair.Cell & bioscience · 2020Review
- Suppression of autophagy during mitosis via CUL4-RING ubiquitin ligases-mediated WIPI2 polyubiquitination and proteasomal degradation.Autophagy · 2019Article
- Inhibition of neddylation induces mitotic defects and alters MKLP1 accumulation at the midbody during cytokinesis.Cell cycle (Georgetown, Tex.) · 2019Article
- The Nedd8-activating enzyme inhibitor MLN4924 (TAK-924/Pevonedistat) induces apoptosis via c-Myc-Noxa axis in head and neck squamous cell carcinoma.Cell proliferation · 2019Article
- Targeting inhibitors of apoptosis proteins suppresses medulloblastoma cell proliferation via G2/M phase arrest and attenuated neddylation of p21.Cancer medicine · 2018Article
- Protein neddylation and its alterations in human cancers for targeted therapy.Cellular signalling · 2018Review
- The SKP1-Cullin-F-box E3 ligase βTrCP and CDK2 cooperate to control STIL abundance and centriole number.Open biology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 1 institution.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The first-in-class compound MLN4924 is a small molecule inhibitor that selectively inactivates NEDD8-activating enzyme (NAE). The anticancer effects of MLN4924 have been attributed to impaired neddylation of Cullin proteins. Here, we show that treatment of T-cell acute lymphoblastic leukemia (T-ALL) cells with MLN4924 potently suppressed the neddylation of Cullins and the oncogenic growth of T-ALL cells in-vitro. Moreover, MLN4924 induced disease regression in an in vivo xenograft model. MLN4924 also induced cell cycle arrest at G2 phase and apoptosis in T-ALL cells. However, inhibition of the neddylation of Cullins alone could not explain the effects of MLN4924 in T-ALL cells. Gene expression profiling indicated ribosome function, steroid biosynthesis, and hematopoietic cell lineage pathways were affected by MLN4924 treatment. MLN4924 also induced nucleolar disruption, suggesting nucleolar stress signaling might contribute to the anticancer effects of MLN4924 in T-ALL cells. In addition, MLN4924 treatment reduced 14-3-3ξ\δ protein levels in T-ALL cells. Thus, MLN4924 may inhibit T-ALL cell proliferation via several pathways.
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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.