ArticleLeukemia2017
JUN is a key transcriptional regulator of the unfolded protein response in acute myeloid leukemia.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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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
60 citing papers in PubMed, 109 citations in OpenAlex.
- Quizartinib and omacetaxine mepesuccinate combination therapy in FLT3-ITD AML: a phase II trial.Nature communications · 2026Trial
- Transcriptome and Regulatory Network Analyses of CD19-CAR-T Immunotherapy for B-ALL.Genomics, proteomics & bioinformatics · 2019Trial
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- ATF4 coordinates amino acid and nucleotide synthesis with selective protein translation to ensure proper DNA replication timing in leukemia cells.Nature communications · 2026Article
- Celastrol induces apoptosis of myelodysplastic syndrome cells through a ROS-dependent pro-apoptotic endoplasmic-reticulum stress pathway.Cancer cell international · 2026Article
- Self-polymerized polyphenol-based platform for the management of dry eye pathogenesis.Nature communications · 2026Article
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- BCLAF1 links RNA splicing to ATF4-dependent metabolic adaptation in acute myeloid leukemia.bioRxiv : the preprint server for biology · 2026Article
- Single-cell RNA-seq reveals the piperlongumine is a potential drug for ischemic stroke.PloS one · 2026Article
- The PERK signaling pathway as a marker of the unfolded protein response in patients with acute myeloid leukemia.Turkish journal of medical sciences · 2026Article
- How to drug a leukemic stem cell: deciphering heterogeneity for better specificity.Blood neoplasia · 2025Review
- Upregulation of ALDH1 as an adaptive epigenetic response to anthracyclines in acute myeloid leukemia.HemaSphere · 2025Article
- CXCL12 chemokine dimer signaling modulates acute myelogenous leukemia cell migration through altered receptor internalization.Scientific reports · 2025Article
- Establishment of a prognostic model based on ER stress-related cell death genes and proposing a novel combination therapy in acute myeloid leukemia.Journal of translational medicine · 2025Article
- scRNA-seq reveals an immune microenvironment and JUN-mediated NK cell exhaustion in relapsed T-ALL.Cell reports. Medicine · 2025Article
- Endoplasmic Reticulum Stress in Acute Myeloid Leukemia: Pathogenesis, Prognostic Implications, and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Identification of a novel unfolded protein response related signature for predicting the prognosis of acute myeloid leukemia.Scientific reports · 2025Article
- Transcriptome Analysis Reveals the Molecular Mechanism of PLIN1 in Goose Hierarchical and Pre-Hierarchical Follicle Granulosa Cells.Animals : an open access journal from MDPI · 2025Article
- Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
The transcription factor JUN is frequently overexpressed in multiple genetic subtypes of acute myeloid leukemia (AML); however, the functional role of JUN in AML is not well defined. Here we report that short hairpin RNA (shRNA)-mediated inhibition of JUN decreases AML cell survival and propagation in vivo. By performing RNA sequencing analysis, we discovered that JUN inhibition reduces the transcriptional output of the unfolded protein response (UPR), an intracellular signaling transduction network activated by endoplasmic reticulum (ER) stress. Specifically, we found that JUN is activated by MEK signaling in response to ER stress, and that JUN binds to the promoters of several key UPR effectors, such as XBP1 and ATF4, to activate their transcription and allow AML cells to properly negotiate ER stress. In addition, we observed that shRNA-mediated inhibition of XBP1 or ATF4 induces AML cell apoptosis and significantly extends disease latency in vivo tying the reduced survival mediated by JUN inhibition to the loss of pro-survival UPR signaling. These data uncover a previously unrecognized role of JUN as a regulator of the UPR as well as provide key new insights into the how ER stress responses contribute to AML and identify JUN and the UPR as promising therapeutic targets in this disease.
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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.