ArticleMolecular cancer research : MCR2010
Sustained c-Jun-NH2-kinase activity promotes epithelial-mesenchymal transition, invasion, and survival of breast cancer cells by regulating extracellular signal-regulated kinase activation.
Article in Molecular cancer research : MCR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 82 citations in OpenAlex.
- Polydopamine-Coated Surfaces Promote Adhesion, Migration, Proliferation, Chemoresistance, Stemness, and Epithelial-Mesenchymal Transition of Human Prostate Cancer Cell Lines In Vitro via Integrin αInternational journal of molecular sciences · 2026Article
- Modulators of epithelial-mesenchymal transitions in prostate cancer: potential for novel therapeutics development.Frontiers in pharmacology · 2026Article
- Review
- Synergistic roles of NFATc1 and c-Jun in immunomodulation.Biochemistry and biophysics reports · 2025Review
- The kinase ERK plays a conserved dominant role in the heterogeneity of epithelial-mesenchymal transition in pancreatic cancer cells.Science signaling · 2025Article
- PKC-International journal of molecular sciences · 2025Article
- Article
- ERK3/MAPK6 promotes triple-negative breast cancer progression through collective migration and EMT plasticity.Frontiers in oncology · 2025Article
- GLUT3 Promotes Epithelial-Mesenchymal Transition via TGF-β/JNK/ATF2 Signaling Pathway in Colorectal Cancer Cells.Biomedicines · 2022Article
- Phosphate Toxicity and Epithelial to Mesenchymal Transition.Advances in experimental medicine and biology · 2022Article
- Inflammatory Breast Cancer: The Secretome of HCMVFrontiers in oncology · 2022Article
- Baicalin alleviates chronic obstructive pulmonary disease through regulation of HSP72-mediated JNK pathway.Molecular medicine (Cambridge, Mass.) · 2021Article
- Fluid Shear Stress Induces EMT of Circulating Tumor Cells via JNK Signaling in Favor of Their Survival during Hematogenous Dissemination.International journal of molecular sciences · 2020Article
- Article
- Galectins and Ovarian Cancer.Cancers · 2020Review
- Article
- JNK2 Is Required for the Tumorigenic Properties of Melanoma Cells.ACS chemical biology · 2019Article
- Matrix Hyaluronan-CD44 Interaction Activates MicroRNA and LncRNA Signaling Associated With Chemoresistance, Invasion, and Tumor Progression.Frontiers in oncology · 2019Review
- Article
- Effects of WD‑3 on tumor growth and the expression of integrin αvβ3 and ERK1/2 in mice bearing human gastric cancer using the 18F‑RGD PET/CT imaging system.Molecular medicine reports · 2017Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
The c-Jun NH(2)-terminus kinase (JNK) mediates stress-induced apoptosis and the cytotoxic effect of anticancer therapies. Paradoxically, recent clinical studies indicate that elevated JNK activity in human breast cancer is associated with poor prognosis. Here, we show that overexpression of a constitutively active JNK in human breast cancer cells did not cause apoptosis, but actually induced cell migration and invasion, a morphologic change associated with epithelial-mesenchymal transition (EMT), expression of mesenchymal-specific markers vimentin and fibronectin, and activity of activator protein transcription factors. Supporting this observation, mouse mammary tumor cells that have undergone EMT showed upregulated JNK activity, and the EMT was reversed by JNK inhibition. Sustained JNK activity enhanced insulin receptor substrate-2-mediated ERK activation, which in turn increased c-Fos expression and activator protein activity. In addition, hyperactive JNK attenuated the apoptosis of breast cancer cells treated by the chemotherapy drug paclitaxel, which is in contrast to the requirement for inducible JNK activity in response to cytotoxic chemotherapy. Blockade of extracellular signal-regulated kinase activity diminished hyperactive JNK-induced cell invasion and survival. Our data suggest that the role of JNK changes when its activity is elevated persistently above the basal levels associated with cell apoptosis, and that JNK activation may serve as a marker of breast cancer progression and resistance to cytotoxic drugs.
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