ArticleFrontiers in immunology2025
Disrupting β-Catenin/BCL9 interaction with a peptide prodrug boosts immunotherapy in colorectal cancer.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Beyond the barrier: Engineering the tumor-immune-soil nexus-a mechanistic blueprint for integrating Traditional Chinese Medicine with immunotherapy in metastatic colorectal cancer.Medical oncology (Northwood, London, England) · 2026Review
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Authors and funding
7 authors.
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Abstract
Introduction: Hyperactivation of the Wnt/β-catenin pathway serves as a central mechanism underlying tumor progression, immune evasion, and resistance to immune checkpoint inhibitor therapy in colorectal cancer (CRC). A pivotal contributor to this process is the binding of β-catenin to B-cell lymphoma 9 (BCL9), which promotes transcription of oncogenes and fosters an immune-suppressive tumor milieu. Consequently, targeting this interaction offers a promising approach to suppress tumor progression and potentiate antitumor immune responses. Methods: We developed a peptide-based prodrug, Bcl9@TP, designed to competitively bind the BCL9 interface on β-catenin, destabilize the transcriptional complex, and suppress Wnt/β-catenin signaling. Its antitumor efficacy and immune potentiation were assessed Results: Discussion: Our findings indicate that disrupting the β-catenin/BCL9 interaction with a peptide-based nanoprodrug represents a compelling strategy to suppress oncogenic signaling and enhance immunotherapy responses in CRC, providing a new angle to boost checkpoint sensitivity.
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