• CLINT1 is specifically upregulated in LUAD but not in LUSC, at both mRNA and protein levels.
• High CLINT1 expression is associated with poor overall and first-progression survival in LUAD patients.
• CLINT1 acts as a downstream effector of p53-R273H, mediating its pro-migratory effects in LUAD.
• Targeting CLINT1 may offer a novel therapeutic strategy for LUAD, especially in p53-R273H-mutant tumors.
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