ArticleNucleic acids research2014
MYC and EGR1 synergize to trigger tumor cell death by controlling NOXA and BIM transcription upon treatment with the proteasome inhibitor bortezomib.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 64 citations in OpenAlex.
- Mutational Spectrum, Copy Number Changes, and Outcome: Results of a Sequencing Study of Patients With Newly Diagnosed Myeloma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2015Trial
- An FDA-approved drug library screening identifies proteasome inhibitors as selective cytotoxic agents for angiosarcoma cells.British journal of cancer · 2025Review
- Single-molecule RNA-FISH analysis reveals stochasticity in reactivation of latent HIV-1 regulated by Nuclear Orphan Receptors NR4A and cMYC.Research square · 2024Article
- Review
- Article
- Article
- EGR1 Haploinsufficiency Confers a Fitness Advantage to Hematopoietic Stem Cells Following Chemotherapy.Experimental hematology · 2022Article
- Targeting the MYC interaction network in B-cell lymphoma via histone deacetylase 6 inhibition.Oncogene · 2022Article
- Article
- Activated SUMOylation restricts MHC class I antigen presentation to confer immune evasion in cancer.The Journal of clinical investigation · 2022Article
- NOXA expression drives synthetic lethality to RUNX1 inhibition in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Z-Ligustilide Induces c-Myc-Dependent ApoptosisFrontiers in oncology · 2022Article
- Deuterium Oxide (DCancers · 2021Article
- Article
- Ubiquitination and Ubiquitin-Like Modifications in Multiple Myeloma: Biology and Therapy.Cancers · 2020Review
- Targeting the ubiquitin-proteasome system in a pancreatic cancer subtype with hyperactive MYC.Molecular oncology · 2020Article
- c-MYC expression and maturity phenotypes are associated with outcome benefit from addition of ixazomib to lenalidomide-dexamethasone in myeloma.European journal of haematology · 2020Article
- Reversal of glucocorticoid resistance in paediatric acute lymphoblastic leukaemia is dependent on restoring BIM expression.British journal of cancer · 2020Article
- Herbal formula Yangyinjiedu induces lung cancer cell apoptosis via activation of early growth response 1.Journal of cellular and molecular medicine · 2019Article
- Overexpressing miR‑335 inhibits DU145 cell proliferation by targeting early growth response 3 in prostate cancer.International journal of oncology · 2019Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-MYC (MYC afterward) oncogene is well known for driving numerous oncogenic programs. However, MYC can also induce apoptosis and this function of MYC warrants further clarification. We report here that a clinically relevant proteasome inhibitor significantly increases MYC protein levels and that endogenous MYC is necessary for the induction of apoptosis. This kind of MYC-induced cell death is mediated by enhanced expression of the pro-apoptotic BCL2 family members NOXA and BIM. Quantitative promoter-scanning chromatin immunoprecipitations (qChIP) further revealed binding of MYC to the promoters of NOXA and BIM upon proteasome inhibition, correlating with increased transcription. Both promoters are further characterized by the presence of tri-methylated lysine 4 of histone H3, marking active chromatin. We provide evidence that in our apoptosis models cell death occurs independently of p53 or ARF. Furthermore, we demonstrate that recruitment of MYC to the NOXA as well as to the BIM gene promoters depends on MYC's interaction with the zinc finger transcription factor EGR1 and an EGR1-binding site in both promoters. Our study uncovers a novel molecular mechanism by showing that the functional cooperation of MYC with EGR1 is required for bortezomib-induced cell death. This observation may be important for novel therapeutic strategies engaging the inherent pro-death function of MYC.
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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.