ArticleBiomaterials research2026
Mesothelin-Binding Peptide Inhibits Cell Migration and Enables Targeted Delivery of a Mitochondrial-Membrane-Damaging Peptide to Pancreatic Tumors.
Article in Biomaterials research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Authors and funding
15 authors.
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Abstract
Mesothelin (MSLN) is up-regulated in many tumors, including pancreatic tumors, making it a promising therapeutic target. We used a phage-displayed peptide library to identify an MSLN-binding peptide. CTILWSLTC, synthesized in cyclic form (MSLNpep), was selected from the library. MSLNpep bound preferentially to MSLN-high versus MSLN-low cells, internalized efficiently, and bound recombinant MSLN more strongly than a control peptide. MSLNpep treatment reduced migration and invasion in MSLN-high tumor cells. To enable targeted cytotoxicity, we generated chimeras linking MSLNpep to L-form or D-form mitochondrial-membrane-damaging peptides (MSLNpep-KLA and MSLNpep-kla, respectively). MSLNpep-kla-and, to a lesser extent, MSLNpep-KLA-exhibited selective cytotoxicity toward MSLN-high versus MSLN-low cells. Systemic MSLNpep-kla, but not MSLNpep-KLA, suppressed orthotopic pancreatic tumor growth, increased survival, and produced no detectable hepatic or renal toxicity in mice. MSLNpep-kla also induced cytotoxicity in patient-derived pancreatic cancer organoids proportionate to MSLN expression. Analysis of a public single-cell RNA-sequencing dataset of human pancreatic cancer tissues revealed that
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