ArticleCancer research2014
Impaired JNK signaling cooperates with KrasG12D expression to accelerate pancreatic ductal adenocarcinoma.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 32 citations in OpenAlex.
- Drivers of Pancreatic Cancer: Beyond the Big 4.Cancers · 2025Review
- Deletion of 17p in cancers: Guilt by (p53) association.Oncogene · 2025Review
- Pharmacological inhibition of the MAP2K7 kinase in human disease.Frontiers in oncology · 2024Review
- HER2-driven breast cancer suppression by the JNK signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- JNK inhibitor IX restrains pancreatic cancer through p53 and p21.Frontiers in oncology · 2022Article
- The MK2/Hsp27 axis is a major survival mechanism for pancreatic ductal adenocarcinoma under genotoxic stress.Science translational medicine · 2021Article
- Spatio-temporal expression pattern and role of the tight junction protein MarvelD3 in pancreas development and function.Scientific reports · 2021Article
- Dysregulated SREBP1c/miR-153 signaling induced by hypertriglyceridemia worsens acute pancreatitis and delays tissue repair.JCI insight · 2021Article
- Loss of c-Jun N-terminal Kinase 1 and 2 Function in Liver Epithelial Cells Triggers Biliary Hyperproliferation Resembling Cholangiocarcinoma.Hepatology communications · 2020Article
- Irreversible JNK1-JUN inhibition by JNK-IN-8 sensitizes pancreatic cancer to 5-FU/FOLFOX chemotherapy.JCI insight · 2020Article
- Saikosaponin D Inhibits Proliferation and Promotes Apoptosis Through Activation of MKK4-JNK Signaling Pathway in Pancreatic Cancer Cells.OncoTargets and therapy · 2020Article
- Ten hub genes associated with progression and prognosis of pancreatic carcinoma identified by co-expression analysis.International journal of biological sciences · 2018Article
- Novel tumor-suppressor function of KLF4 in pediatric T-cell acute lymphoblastic leukemia.Experimental hematology · 2017Review
- miR-125b expression affects tumor growth of multiple myeloma via targeting MKK7.International journal of clinical and experimental pathology · 2017Article
- Article
- The MKK7 p.Glu116Lys Rare Variant Serves as a Predictor for Lung Cancer Risk and Prognosis in Chinese.PLoS genetics · 2016Article
- GEMMs as preclinical models for testing pancreatic cancer therapies.Disease models & mechanisms · 2015Review
- Inhibition of JNK Sensitizes Hypoxic Colon Cancer Cells to DNA-Damaging Agents.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Article
- In vivo gene manipulation reveals the impact of stress-responsive MAPK pathways on tumor progression.Cancer science · 2015Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The c-Jun N-terminal protein kinase (JNK) and its two direct activators, namely the mitogen-activated protein kinase (MAPK) kinase 4 (MKK4) and MKK7, constitute a signaling node frequently mutated in human pancreatic ductal adenocarcinoma (PDAC). Here we demonstrate the cooperative interaction of endogenous expression of Kras(G12D) with loss-of-function mutations in mkk4 or both, mkk4 and mkk7 genes in the pancreas. More specifically, impaired JNK signaling in a subpopulation of Pdx1-expressing cells dramatically accelerated the appearance of Kras(G12D)-induced acinar-to-ductal metaplasia and pancreatic intraepithelial neoplasias, which rapidly progressed to invasive PDAC within 10 weeks of age. Furthermore, inactivation of mkk4/mkk7 compromised acinar regeneration following acute inflammatory stress by locking damaged exocrine cells in a permanently de-differentiated state. Therefore, we propose that JNK signaling exerts its tumor suppressive function in the pancreas by antagonizing the metaplastic conversion of acinar cells toward a ductal fate capable of responding to oncogenic stimulation.
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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.