ArticleCell death & disease2025
Decoy-PROTAC for specific degradation of "Undruggable" STAT3 transcription factor.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed.
- PROTACs in cancer therapy: targeted degradation of GPX4, PARP and epigenetic regulators.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- Targeted degradation of protein in hematologic malignancies: mechanisms, therapeutic strategies, and clinical prospects.Cancer gene therapy · 2026Review
- STAT3 signaling inhibitors for cancer treatment.Trends in pharmacological sciences · 2026Review
- Precision-Engineered PROTACs: Integrating Physical and Chemical Strategies for Targeted Cancer Therapy.Small (Weinheim an der Bergstrasse, Germany) · 2026Review
- Proteolysis-targeting chimera (PROTAC) in cancer: design principles and applications on "undruggable" targets.Biomarker research · 2026Review
- Combining Small-Molecular Compounds With CAR T-Cell Therapy: Novel Strategies for Enhanced Cancer Immunotherapy.Cancer innovation · 2026Review
- Psoralen and Isopsoralen fromPharmaceuticals (Basel, Switzerland) · 2026Article
- Advances in protein ubiquitination modification and immune evasion of breast cancer.Frontiers in cell and developmental biology · 2026Review
- Role of the SOX family in non‑small cell lung cancer: Molecular mechanisms and therapeutic implications (Review).Oncology reports · 2026Review
- Discovery of a potent STAT3 inhibitor WR-S-647 for the treatment of ADPKD.Archives of pharmacal research · 2026Article
- IL-1β-induced STAT3 activation drives IL-17-producing CD8Journal of translational medicine · 2025Article
- Recent advances in targeting protein degradation for tumor immunotherapy.Journal of hematology & oncology · 2025Review
- Next-Generation Proteolysis-Targeting Chimeras in Precision Oncology: Multifunctional Designs, Emerging Modalities, and Translational Prospects in Targeted Protein Degradation.Drug development research · 2025Review
- STAT3 axis in cancer and cancer stem cells: From oncogenesis to targeted therapies.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signal transducer and activator of transcription 3 (STAT3) is widely recognized as an attractive target for cancer therapy due to its significant role in the initiation and progression of tumorigenesis. However, existing STAT3 inhibitors have suffered from drawbacks including poor efficacy, limited specificity, and undesirable off-target effects, due to the challenging nature of identifying active sites or allosteric regulatory pockets on STAT3 amenable to small-molecule inhibition. In response to these obstacles, we utilize the innovative proteolysis targeting chimera (PROTAC) technology to create a highly specific decoy-targeted protein degradation system for STAT3 protein, termed D-PROTAC. This system fuses DNA decoy that targets STAT3 with an E3 ligase ligand, utilizing a click chemistry approach. Experimental results demonstrate that D-PROTAC efficiently mediates the degradation of the STAT3 protein across various cancer cell types, leading to the downregulation of crucial downstream STAT3 targets, inhibiting tumor cell growth, triggering cell cycle arrest and apoptosis, and suppressing tumor immune evasion. Furthermore, D-PROTAC is capable of achieving significant tumor suppression in xenograft models. Overall, our research validates that D-PROTAC can successfully target and eliminate the "undruggable" STAT3, showcasing specificity and potent antitumor effects. This strategy will suggest a promising avenue for the development of targeted therapies against the critical functions of STAT3 in human cancers and potentially other diseases.
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Registered trials
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.