ArticleMolecular and cellular biology2011
Requirement of c-Jun NH(2)-terminal kinase for Ras-initiated tumor formation.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 96 citations in OpenAlex.
- Transcriptome profiling and metabolic pathway analysis towards reliable biomarker discovery in early-stage lung cancer.Journal of applied genetics · 2025Article
- Oncogenic KRAS Drives Lipofibrogenesis to Promote Angiogenesis and Colon Cancer Progression.Cancer discovery · 2023Article
- Mutant Ras and inflammation-driven skin tumorigenesis is suppressed via a JNK-iASPP-AP1 axis.Cell reports · 2022Article
- DUSP4 Silencing Enhances the Sensitivity of Breast Cancer Cells to Doxorubicin through the Activation of the JNK/c-Jun Signalling Pathway.Molecules (Basel, Switzerland) · 2022Article
- Metastasis and MAPK Pathways.International journal of molecular sciences · 2022Review
- JNK inhibitor IX restrains pancreatic cancer through p53 and p21.Frontiers in oncology · 2022Article
- U0126: Not only a MAPK kinase inhibitor.Frontiers in pharmacology · 2022Review
- Dissection of the Regulatory Elements of the Complex Expression Pattern of Puckered, a Dual-Specificity JNK Phosphatase.International journal of molecular sciences · 2021Article
- K15 promoter-driven enforced expression of NKIRAS exhibits tumor suppressive activity against the development of DMBA/TPA-induced skin tumors.Scientific reports · 2021Article
- Stress-activated kinases as therapeutic targets in pancreatic cancer.World journal of gastroenterology · 2021Review
- JunD, not c-Jun, is the AP-1 transcription factor required for Ras-induced lung cancer.JCI insight · 2021Article
- Article
- JNK in Tumor Microenvironment: Present Findings and Challenges in Clinical Translation.Cancers · 2021Review
- E6-mediated activation of JNK drives EGFR signalling to promote proliferation and viral oncoprotein expression in cervical cancer.Cell death and differentiation · 2021Article
- Hsa-miR-557 Inhibits Osteosarcoma Growth Through Targeting KRAS.Frontiers in genetics · 2021Article
- Loss of c-Jun N-terminal Kinase 1 and 2 Function in Liver Epithelial Cells Triggers Biliary Hyperproliferation Resembling Cholangiocarcinoma.Hepatology communications · 2020Article
- JNK Signaling in Stem Cell Self-Renewal and Differentiation.International journal of molecular sciences · 2020Review
- Activation of PERK Contributes to Apoptosis and GCancers · 2019Article
- JNK2 Is Required for the Tumorigenic Properties of Melanoma Cells.ACS chemical biology · 2019Article
- JNKNature communications · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The c-Jun NH(2)-terminal kinase (JNK) signal transduction pathway causes increased gene expression mediated, in part, by members of the activating transcription factor protein (AP1) group. JNK is therefore implicated in the regulation of cell growth and cancer. To test the role of JNK in Ras-induced tumor formation, we examined the effect of compound ablation of the ubiquitously expressed genes Jnk1 plus Jnk2. We report that JNK is required for Ras-induced transformation of p53-deficient primary cells in vitro. Moreover, JNK is required for lung tumor development caused by mutational activation of the endogenous KRas gene in vivo. Together, these data establish that JNK plays a key role in Ras-induced tumorigenesis.
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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.