ArticleAnimal cells and systems2025
Targeting MMR-deficient colorectal cancer with a potent small molecule UNI110.
Article in Animal cells and systems, 2025. 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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Abstract
Mismatch repair (MMR) deficiency is a hallmark of microsatellite instability (MSI) in hereditary non-polyposis colorectal cancer, Lynch syndrome, contributing to resistance against conventional chemotherapy and posing a significant therapeutic challenge. In this study, we introduce UNI110, a novel small molecule derived from Baicalein, engineered for enhanced selectivity against MMR-deficient cancer cells. UNI110 exhibits a remarkable sevenfold increase in potency over Baicalein, demonstrating significantly lower IC50 values and heightened cytotoxic effects in MMR-deficient cell lines. Mechanistically, UNI110 selectively induces DNA damage in MMR-deficient cancer cells, ultimately resulting in cell death. Furthermore, UNI110 disrupts homologous recombination (HR) repair by inhibiting the MSH2-MSH3 complex, specifically blocking the interaction between MSH2 and EXO1, thereby impairing long-range end resection during double-strand break (DSB) repair. These findings establish UNI110 as a promising lead compound for the targeted treatment of MMR-deficient colorectal cancers, offering a potential breakthrough in overcoming chemotherapy resistance and improving patient outcomes.
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