ArticleScientific reports2016
TAK1 inhibitor NG25 enhances doxorubicin-mediated apoptosis in breast cancer cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- M-GNN: A Topology-Enhanced Multi-Modal Graph Neural Network for Cancer Driver Gene Prediction.Metabolites · 2026Article
- NG25 Enhances Anti-Tumor Immunity inOncoTargets and therapy · 2026Article
- The Trim32-DPEP2 axis is an inflammatory switch in macrophages during intestinal inflammation.Cell death and differentiation · 2025Article
- Exploration of crucial stromal risk genes associated with prognostic significance and chemotherapeutic opportunities in invasive ductal breast carcinoma.Journal, genetic engineering & biotechnology · 2025Article
- Synergistic Potential of GLP-1 Receptor Agonists and Radiotherapy in Breast Cancer Treatment: A New Therapeutic Avenue (TROD-GROG 006).Current radiopharmaceuticals · 2025Article
- Suppression of triple-negative breast cancer aggressiveness by LGALS3BP via inhibition of the TNF-α-TAK1-MMP9 axis.Cell death discovery · 2023Article
- Semisynthesis of Hypothemycin Analogues Targeting the C8-C9 Diol.Journal of natural products · 2022Review
- TGF-β-activated kinase-1 inhibitor LL-Z1640-2 reduces joint inflammation and bone destruction in mouse models of rheumatoid arthritis by inhibiting NLRP3 inflammasome, TACE, TNF-α and RANKL expression.Clinical & translational immunology · 2022Article
- Review
- Tumor resistance to radiotherapy is triggered by an ATM/TAK1-dependent-increased expression of the cellular prion protein.Oncogene · 2021Article
- Discovery of 2,4-1ACS medicinal chemistry letters · 2021Article
- USP1-WDR48 deubiquitinase complex enhances TGF-β induced epithelial-mesenchymal transition of TNBC cells via stabilizing TAK1.Cell cycle (Georgetown, Tex.) · 2021Article
- ARRB1 Drives Gallbladder Cancer Progression by Facilitating TAK1/MAPK Signaling Activation.Journal of Cancer · 2021Article
- Six-Transmembrane Epithelial Antigen of the Prostate 3 Deficiency in Hepatocytes Protects the Liver Against Ischemia-Reperfusion Injury by Suppressing Transforming Growth Factor-β-Activated Kinase 1.Hepatology (Baltimore, Md.) · 2020Article
- TLR2 Signaling Pathway CombatsCells · 2020Article
- NG25, a novel inhibitor of TAK1, suppresses KRAS-mutant colorectal cancer growth in vitro and in vivo.Apoptosis : an international journal on programmed cell death · 2019Article
- Topological alternate centrality measure capturing drug targets in the network of MAPK pathways.IET systems biology · 2018Article
- Doxorubicin induces an extensive transcriptional and metabolic rewiring in yeast cells.Scientific reports · 2018Article
- SIRT7 depletion inhibits cell proliferation, migration, and increases drug sensitivity by activating p38MAPK in breast cancer cells.Journal of cellular physiology · 2018Article
- TAK1 mediates microenvironment-triggered autocrine signals and promotes triple-negative breast cancer lung metastasis.Nature communications · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (Dox, Adriamycin) has been widely used in breast cancer treatment. But its severe cardio-toxic side effects limited the clinical use. Dox treatment can induce DNA damage and other accompanying effects in cancer cells, and subsequently activates nuclear factor κB (NF-κB) pathway which has a strong pro-survival role in different types of malignancy. We hypothesize that blocking NF-κB pathway may sensitize breast cancer cells to Dox chemotherapy. TGFβ-activated kinase-1 (TAK1) is a key intracellular molecule participating in genotoxic stresses-induced NF-κB activation. Targeting TAK1 as a strategy to enhance cancer treatment efficacy has been studied in several malignancies. We showed that NG25, a synthesized TAK1 inhibitor, greatly enhanced Dox treatment efficacy in a panel of breast cancer cell lines. In this pre-clinical study, we found that NG25 partially blocked Dox-induced p38 phosphorylation and IκBα degradation and enhanced Dox-induced cytotoxic effects and apoptosis in all breast cancer cell lines tested. Taken together, we provided clear evidence that NG25 sensitizes the breast cancer cells to Dox treatment in vitro. This combination may be an effective and feasible therapeutic option maximizing Dox efficacy and meanwhile minimizing Dox side effects in treating breast cancer.
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