ArticleOncogene2017
c-Jun N-terminal kinase promotes stem cell phenotype in triple-negative breast cancer through upregulation of Notch1 via activation of c-Jun.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 100 citations in OpenAlex.
- Doxorubicin-Induced Cytotoxicity in Adipose-Derived Stem Cells Is Associated With Altered SAPK/JNK Signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Notch receptors in breast cancer: context-dependent roles and therapeutic targeting.Cell communication and signaling : CCS · 2026Review
- ATR inhibition potentiates the antitumor efficacy of HER3-DXd in HER3-positive/HR-positive breast cancer by increasing DNA damage.British journal of cancer · 2026Article
- MYOD1 mutation drives cancer stem cell pathways and therapy-resistance in spindle cell/sclerosing rhabdomyosarcoma.Nature communications · 2026Article
- α-Viniferin Induces Intrinsic Apoptosis in Triple-Negative Breast Cancer Cells and Synergizes With SB203580 Independently of p38 Mitogen-Activated Protein Kinase.Journal of breast cancer · 2026Article
- Novel pyridine-based chalcone analogs and triple negative breast cancer: potential therapy & molecular pathways.Scientific reports · 2026Article
- Role of immunosuppressive JNK pathway in the tumor microenvironment among TNBC subtypes in IBCSG trial 22-00.iScience · 2025Article
- Targeting CDK7 Enhances the Antitumor Efficacy of Enzalutamide in Androgen Receptor-Positive Triple-Negative Breast Cancer by Inhibiting c-MYC-mediated Tumorigenesis.Molecular cancer therapeutics · 2025Article
- An update on cancer stem cell survival pathways involved in chemoresistance in triple-negative breast cancer.Future oncology (London, England) · 2025Review
- Transplantation of gastric epithelial mitochondria into human gastric cancer cells inhibits tumor growth and enhances chemosensitivity by reducing cancer stemness and modulating gastric cancer metabolism.Stem cell research & therapy · 2025Article
- Identification and validation of genes related to stem cells and telomere maintenance mechanisms as biomarkers for breast cancer.Frontiers in immunology · 2025Article
- Brca1 haploinsufficiency promotes early tumor onset and epigenetic alterations in a mouse model of hereditary breast cancer.Nature genetics · 2024Article
- Article
- TWEAK/Fn14 signalling driven super-enhancer reprogramming promotes pro-metastatic metabolic rewiring in triple-negative breast cancer.Nature communications · 2024Article
- Network-based approach elucidates critical genes in BRCA subtypes and chemotherapy response in triple negative breast cancer.iScience · 2024Article
- Biological Basis of Breast Cancer-Related Disparities in Precision Oncology Era.International journal of molecular sciences · 2024Review
- Aggresome formation promotes ASK1/JNK signaling activation and stemness maintenance in ovarian cancer.Nature communications · 2024Article
- A review of biological targets and therapeutic approaches in the management of triple-negative breast cancer.Journal of advanced research · 2023Review
- MUC1-C intersects chronic inflammation with epigenetic reprogramming by regulating the set1a compass complex in cancer progression.Communications biology · 2023Article
- Targeting c-Jun inhibits fatty acid oxidation to overcome tamoxifen resistance in estrogen receptor-positive breast cancer.Cell death & disease · 2023Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
c-Jun N-terminal kinase (JNK) plays a vital role in malignant transformation of different cancers, and JNK is highly activated in basal-like triple-negative breast cancer (TNBC). However, the roles of JNK in regulating cancer stem-like cell (CSC) phenotype and tumorigenesis in TNBC are not well defined. JNK is known to mediate many cellular events via activating c-Jun. Here, we found that JNK regulated c-Jun activation in TNBC cells and that JNK activation correlated with c-Jun activation in TNBC tumors. Furthermore, the expression level of c-Jun was significantly higher in TNBC tumors than in non-TNBC tumors, and high c-Jun mRNA level was associated with shorter disease-free survival of patients with TNBC. Thus, we hypothesized that the JNK/c-Jun signaling pathway contributes to TNBC tumorigenesis. We found that knockdown of JNK1 or JNK2 or treatment with JNK-IN-8, an adenosine triphosphate-competitive irreversible pan-JNK inhibitor, significantly reduced cell proliferation, the ALDH1
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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.