ArticleHistochemistry and cell biology2015
c-Jun N-terminal kinase inhibitor SP600125 enhances barrier function and elongation of human pancreatic cancer cell line HPAC in a Ca-switch model.
Article in Histochemistry and cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting the MAPK Pathway in Cancer.International journal of molecular sciences · 2025Review
- LSR antibody promotes apoptosis and disrupts epithelial barriers via signal pathways in endometrial cancer.Tissue barriers · 2023Article
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- Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma.International journal of molecular sciences · 2022Review
- 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
- Cytoskeleton and Associated Proteins: Pleiotropic JNK Substrates and Regulators.International journal of molecular sciences · 2021Review
- Porcine circovirus type 2 exploits JNK-mediated disruption of tight junctions to facilitate Streptococcus suis translocation across the tracheal epithelium.Veterinary research · 2020Article
- Epithelial barrier dysfunction and cell migration induction via JNK/cofilin/actin by angubindin-1.Tissue barriers · 2020Article
- JNK, p38, ERK, and SGK1 Inhibitors in Cancer.Cancers · 2017Article
- Salmonella enteritidis Effector AvrA Stabilizes Intestinal Tight Junctions via the JNK Pathway.The Journal of biological chemistry · 2016Article
- Article
- The Histochemistry and Cell Biology omnium-gatherum: the year 2015 in review.Histochemistry and cell biology · 2016Review
- F-actin binding protein, anillin, regulates integrity of intercellular junctions in human epithelial cells.Cellular and molecular life sciences : CMLS · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
c-Jun N-terminal kinase (JNK), known as a stress-activated protein kinase, regulates normal epithelial biological processes, including assembly of adherens and tight junctions, and it is involved in the development of several cancers. The JNK inhibitor SP600125 enhances epithelial barrier function through modulation of tight junction molecules in normal human pancreatic epithelial cells. Furthermore, this JNK inhibitor suppresses the growth of human pancreatic cancer cells. However, the effects of SP600125 on the epithelial barrier in human pancreatic cancer cells remain unknown. In the present study, the JNK inhibitor SP600125 markedly enhanced the barrier function and cell elongation of well-differentiated human pancreatic cancer cell line HPAC in a Ca-switch model. The epithelial barrier function induced by SP600125 was regulated by phosphorylated β-catenin without changes in the tight junction molecules. The cell elongation induced by SP600125 was closely related to the expression of the F-actin-binding protein DrebrinE. These findings suggest that JNK is involved in the regulation of the epithelial barrier function and cell shape during remodeling of pancreatic cancer cells. The JNK inhibitor SP600125 may have potential as a therapeutic drug for pancreatic cancer via induction of differentiation.
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