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Blocking αvβ3/galectin-3 binding with GCS-100 selectively kills KRAS-addicted lung cancer cells. Blocking αvβ3/galectin-3 binding with GCS-100 selectively.

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Presentation on theme: "Blocking αvβ3/galectin-3 binding with GCS-100 selectively kills KRAS-addicted lung cancer cells. Blocking αvβ3/galectin-3 binding with GCS-100 selectively."— Presentation transcript:

1 Blocking αvβ3/galectin-3 binding with GCS-100 selectively kills KRAS-addicted lung cancer cells.
Blocking αvβ3/galectin-3 binding with GCS-100 selectively kills KRAS-addicted lung cancer cells. A and B, A cell-free binding assay shows direct binding between integrin αvβ3 and galectin-3, and its competitive inhibition by lactose. C, A galectin-3 inhibitor, GCS-100, disrupts αvβ3/galectin-3 binding in the cell-free assay. D, Flow cytometer analysis for cell surface galectin-3 expression. E and F, The effect of GCS-100 on 3-D viability of KRAS-mutant lung cancer cell lines and PDX models is enhanced by αvβ3 expression. G, Embryonic fibroblasts from genetically engineered mice [wild-type, KrasG12D, Lgals3 knockout (KO), or the combination] were compared for sensitivity to GCS-100. All data represent mean ± SD from at least three independent experiments. Statistical significance was determined by the Student t test. *, P < 0.05; **, P < 0.01. Laetitia Seguin et al. Cancer Discov 2017;7: ©2017 by American Association for Cancer Research

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