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Laetitia Seguin is currently working as a postdoctoral fellow in C Feral Laboratory Epithelial homeostasis and tumorigenesis at IRCAN, France. She has published many papers in the reputed journals with the eminent authors. She has a great publication in the peer reviewed conference proceedings also.
Identifying the molecular basis for cancer cell dependence on oncogenes such as KRAS can provide new opportunities to target these addictions. Here, we identify a novel role for the carbohydrate-binding protein galectin-3 as a lynchpin for KRAS dependence. By directly binding to the cell surface receptor integrin ?v?3, galectin-3 gives rise to KRAS addiction by enabling multiple functions of KRAS in anchorage-independent cells, including formation of macropinosomes that facilitate nutrient uptake and ability to maintain redox balance. Disrupting ?v?3/galectin-3 binding with a clinically active drug prevents their association with mutant KRAS, thereby suppression macropinocytosis while increasing reactive oxygen species to eradicate ?v?3-expressing KRAS-mutant lung and pancreatic cancer patient-derived xenografts and spontaneous tumors in mice. Our work reveals galectin-3 as a druggable target for KRAS-addicted lung and pancreas cancers and indicates integrin ?v?3 as a biomarker to identify susceptible tumors. There is a significant unmet need for therapies targeting KRAS-mutant cancers. Here, we identify integrin ?v?3 as a biomarker to identify mutant KRAS-addicted tumors that are highly sensitive to inhibition of galectin-3, a glycoprotein that binds to integrin ?v?3 to promote KRAS-mediated activation of AKT.