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The adenomatous polyposis coli protein serves as an essential tumor suppressor at both molecular signaling levels—primarily via negative regulation of Wnt/β-catenin—and broader cellular architecture maintenance. Its dysfunction underlies inherited syndromes like FAP as well as most sporadic cases of colon cancer through loss-of-function mutations disrupting these pathways.
Wnt pathway modulation; induction of β-catenin degradation
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