ArticleCancer science2013
Therapeutic effect of c-Jun N-terminal kinase inhibition on pancreatic cancer.
Article in Cancer science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
- Impaired insulin secretion via the Wnt5a/β-catenin pathway contributes to diabetes development in pancreatic cancer.Experimental & molecular medicine · 2026Article
- Blockade of CC chemokine receptor 2 suppresses pancreatic cancer progression through the interaction with macrophages in the tumor microenvironment.Scientific reports · 2025Article
- Bidirectional effects of morphine on pancreatic cancer progression via the p38/JNK pathway.Scientific reports · 2024Article
- GPX3 represses pancreatic cancer cell proliferation, migration and invasion, and improves their chemo‑sensitivity by regulating the JNK/c‑Jun signaling pathway.Experimental and therapeutic medicine · 2024Article
- c-Jun N-terminal kinase signaling in aging.Frontiers in aging neuroscience · 2024Review
- Lipopolysaccharide (LPS) stimulation of Pancreatic Ductal Adenocarcinoma (PDAC) and macrophages activates the NLRP3 inflammasome that influences the levels of pro-inflammatory cytokines in a co-culture model.Cancer biology & therapy · 2023Article
- JNK inhibitor IX restrains pancreatic cancer through p53 and p21.Frontiers in oncology · 2022Article
- Stress-activated kinases as therapeutic targets in pancreatic cancer.World journal of gastroenterology · 2021Review
- JNK signaling as a target for anticancer therapy.Pharmacological reports : PR · 2021Review
- An Overview of Potential Therapeutic Agents Targeting WNT/PCP Signaling.Handbook of experimental pharmacology · 2021Review
- Dysregulated Immune Responses by ASK1 Deficiency Alter Epithelial Progenitor Cell Fate and Accelerate Metaplasia Development duringMicroorganisms · 2020Article
- Major histocompatibility complexes are up-regulated in glomerular endothelial cells via activation of c-Jun N-terminal kinase in 5/6 nephrectomy mice.British journal of pharmacology · 2020Article
- JNK signaling contributes to skeletal muscle wasting and protein turnover in pancreatic cancer cachexia.Cancer letters · 2020Article
- Irreversible JNK1-JUN inhibition by JNK-IN-8 sensitizes pancreatic cancer to 5-FU/FOLFOX chemotherapy.JCI insight · 2020Article
- c-Jun N-terminal kinase in pancreatic tumor stroma augments tumor development in mice.Cancer science · 2017Article
- Downregulation of Human Endogenous Retrovirus Type K (HERV-K) ViralClinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Tenascin-C induces migration and invasion through JNK/c-Jun signalling in pancreatic cancer.Oncotarget · 2017Article
- Histone deacetylase inhibitors provoke a tumor supportive phenotype in pancreatic cancer associated fibroblasts.Oncotarget · 2017Article
- Moscatilin induces apoptosis of pancreatic cancer cells via reactive oxygen species and the JNK/SAPK pathway.Molecular medicine reports · 2017Article
- Smad4 inhibits cell migration via suppression of JNK activity in human pancreatic carcinoma PANC-1 cells.Oncology letters · 2016Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
c-Jun N-terminal kinase (JNK) is a member of the mitogen-activated protein kinase (MAPK) family, and it is reportedly involved in the development of several cancers. However, the role of JNK in pancreatic cancer has not been elucidated. We assessed t he involvement of JNK in the development of pancreatic cancer and investigated the therapeutic effect of JNK inhibitors on this deadly cancer. Small interfering RNAs against JNK or the JNK inhibitor SP600125 were used to examine the role of JNK in cellular proliferation and the cell cycles of pancreatic cancer cell lines. Ptf1a(cre/+) ;LSL-Kras(G12D/+) ;Tgfbr2(flox/flox) mice were treated with the JNK inhibitor to examine pancreatic histology and survival. The effect of JNK inhibition on tumor angiogenesis was also assessed using cell lines and murine pancreatic cancer specimens. JNK was frequently activated in human and murine pancreatic cancer in vitro and in vivo. Growth of human pancreatic cancer cell lines was suppressed by JNK inhibition through G1 arrest in the cell cycle with decreased cyclin D1 expression. In addition, oncogenic K-ras expression led to activation of JNK in pancreatic cancer cell lines. Treatment of Ptf1a(cre/+) ;LSL-Kras(G12D/+) ;Tgfbr2(flox/flox) mice with the JNK inhibitor decreased growth of murine pancreatic cancer and prolonged survival of the mice significantly. Angiogenesis was also decreased by JNK inhibition in vitro and in vivo. In conclusion, activation of JNK promotes development of pancreatic cancer, and JNK may be a potential therapeutic target for pancreatic cancer.
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