ArticleSignal transduction and targeted therapy2025
Precise targeting of transcriptional co-activators YAP/TAZ annihilates chemoresistant brCSCs by alteration of their mitochondrial homeostasis.
Article in Signal transduction and targeted therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Mangiferin in combination with primaquine reduces disease progression and transmission potential while alleviating cerebral pathology through suppression of neural cell apoptosis in experimental cerebral malaria.Inflammopharmacology · 2026Article
- Plasticity of Non-Apoptotic Residual Tumor Cells After Neoadjuvant Immunochemotherapy: Epigenetic and Microenvironmental Determinants.Biomolecules · 2026Review
- METTL16-mediated upregulation of LINC00665 inhibits the apoptosis of breast cancer via regulating miR-28-5p/GLG1 axis.Translational cancer research · 2026Article
- Liquid-liquid phase separation in cancer therapy resistance.iScience · 2026Review
- Hongwu mixture exerts inhibition on triple-negative breast cancer by regulating SAV1/Hippo signaling through ZNF143.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Extracellular matrix signals promote actin-dependent mitochondrial elongation and activity.iScience · 2026Article
- Microglial Fkbp5 Impairs Post-Stroke Vascular Integrity and Regeneration by Promoting Yap1-Mediated Glycolysis and Oxidative Phosphorylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Large-Scaled Proteomics Analysis for Glaucoma: Integrated Genetics, Multi-Omics, UK Biobank and Therapeutic Analysis.Investigative ophthalmology & visual science · 2026Article
- JAM-C prevents ocular fibrosis by suppressing the TAZ/KLF6 pathway.Journal of advanced research · 2026Article
- Targeting mitochondrial homeostasis as a cancer treatment strategy: current status and future prospects.Molecular cancer · 2026Review
- Yes-associated protein 1 in cancer: bridging mechanical transduction and epigenetic regulation.Cancer biology & therapy · 2025Review
- Dysadherin/YAP axis fuels stem plasticity and immune escape in liver cancer.Signal transduction and targeted therapy · 2025Article
- In vitro evaluation of Verteporfin and exploration of TEAD palmitoylation inhibition in Piezo1-YAP/TAZ signaling and ECM remodeling.Scientific reports · 2025Article
- Utility of Multicellular Spheroids for Investigating Mechanisms of Chemoresistance in Triple-Negative Breast Cancer.International journal of molecular sciences · 2025Review
- ER-mitochondria tethering and its signaling: A novel therapeutic target in breast cancer.Molecular therapy. Oncology · 2025Review
- LDHA-mediated YAP lactylation promotes the tumor progression of hepatocellular carcinoma by inducing YAP dephosphorylation and activation.Biology direct · 2025Article
- The Ferroptosis-Mitochondrial Axis in Depression: Unraveling the Feedforward Loop of Oxidative Stress, Metabolic Homeostasis Dysregulation, and Neuroinflammation.Antioxidants (Basel, Switzerland) · 2025Review
- The LRP4/YAP axis drives the radiation-tolerant persister (RTP) cell state in breast cancer.Theranostics · 2025Article
- Targeting Hippo-YAP/TAZ signaling pathway: an updated review demonstrating the therapeutic potential of key plant derived anticancer compounds.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistence of drug-resistant breast cancer stem cells (brCSCs) after a chemotherapeutic regime correlates with disease recurrence and elevated mortality. Therefore, deciphering mechanisms that dictate their drug-resistant phenotype is imperative for designing targeted and more effective therapeutic strategies. The transcription factor SOX2 has been recognized as a protagonist in brCSC maintenance, and previous studies have confirmed that inhibition of SOX2 purportedly eliminated these brCSCs. However, pharmacological targeting of transcription factors like SOX2 is challenging due to their structural incongruities and intrinsic disorders in their binding interfaces. Therefore, transcriptional co-activators may serve as a feasible alternative for effectively targeting the brCSCs. Incidentally, transcriptional co-activators YAP/TAZ were found to be upregulated in CD44
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