ArticleJCI insight2021
JunD, not c-Jun, is the AP-1 transcription factor required for Ras-induced lung cancer.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Local control of Cre-regulated genetic modeling in vivo using wireless implantable optoelectronics.Science advances · 2026Article
- MEN1 Deficiency Drives Lung Cancer Progression via Activation of MMP10-Mediated Angiogenesis.Cancer science · 2026Article
- Multi-omics SMR and experimental supportive analyses decipher causal drivers hepatocellular carcinoma.BMC cancer · 2026Article
- Epigenetic profiling reveals key super-enhancer networks driving oncogenesis in HPV-positive HNSCC.iScience · 2025Article
- Urine Cell-Free RNA vs Plasma Cell-Free RNA for Monitoring of Kidney Injury and Immune Complications.Clinical chemistry · 2025Article
- JUNB and JUND in Urological Cancers: A Literature Review.Current issues in molecular biology · 2025Review
- c-Jun regulates postpartum β-cell apoptosis and survival downstream of prolactin signaling.Molecular and cellular endocrinology · 2025Article
- Article
- Ethyl β-carboline-3-carboxylate targets PRDX5/c-Jun axis for novel therapeutic strategy against cervical cancer.Discover oncology · 2025Article
- Jun, an Oncological Foe or Friend?International journal of molecular sciences · 2025Review
- Granzyme mRNA-miRNA interaction and its implication to functional impact.Genes & genomics · 2024Article
- Review
- The human adenovirus E1B-55K oncoprotein coordinates cell transformation through regulation of DNA-bound host transcription factors.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- p53 inhibitor iASPP is an unexpected suppressor of KRAS and inflammation-driven pancreatic cancer.Cell death and differentiation · 2023Article
- RAS and PP2A activities converge on epigenetic gene regulation.Life science alliance · 2023Article
- Integrated bioinformatics analyses identifying key transcriptomes correlated with prognosis and immune infiltrations in lung squamous cell carcinoma.Saudi journal of biological sciences · 2023Article
- The potential of activator protein 1 (AP-1) in cancer targeted therapy.Frontiers in immunology · 2023Review
- Single-cell RNA-sequencing data analysis reveals a highly correlated triphasic transcriptional response to SARS-CoV-2 infection.Communications biology · 2022Article
- Mutant Ras and inflammation-driven skin tumorigenesis is suppressed via a JNK-iASPP-AP1 axis.Cell reports · 2022Article
- USP28 enables oncogenic transformation of respiratory cells, and its inhibition potentiates molecular therapy targeting mutant EGFR, BRAF and PI3K.Molecular oncology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
The AP-1 transcription factor c-Jun is required for Ras-driven tumorigenesis in many tissues and is considered as a classical proto-oncogene. To determine the requirement for c-Jun in a mouse model of K-RasG12D-induced lung adenocarcinoma, we inducibly deleted c-Jun in the adult lung. Surprisingly, we found that inactivation of c-Jun, or mutation of its JNK phosphorylation sites, actually increased lung tumor burden. Mechanistically, we found that protein levels of the Jun family member JunD were increased in the absence of c-Jun. In c-Jun-deficient cells, JunD phosphorylation was increased, and expression of a dominant-active JNKK2-JNK1 transgene further increased lung tumor formation. Strikingly, deletion of JunD completely abolished Ras-driven lung tumorigenesis. This work identifies JunD, not c-Jun, as the crucial substrate of JNK signaling and oncogene required for Ras-induced lung cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.