APC (Adenomatous Polyposis Coli) is a tumor suppressor gene that encodes a large multifunctional protein.
Its primary role is to regulate the Wnt/β-catenin signaling pathway, which controls cell proliferation, adhesion, and differentiation in epithelial tissues.
APC is essential for maintaining normal colonic epithelium homeostasis.
📊 Prevalence of APC Mutations in Cancer
Cancer Type / Context
APC Mutation Frequency
Colorectal Cancer (sporadic)
~70–80%
Familial Adenomatous Polyposis (FAP)
100% (germline APC mutation)
Gastric Cancer (intestinal subtype)
~10–20%
Hepatocellular Carcinoma
~10%
All cancers (overall)
~5–10%
⚙️ Mechanism: How APC Mutations Cause Cancer
🛡️ Normal APC Function
APC is a key component of the β-catenin destruction complex, which also includes Axin, GSK3β, and CK1.
In the absence of Wnt signaling:
APC helps target β-catenin for degradation.
Prevents excessive transcription of Wnt target genes.
This mechanism keeps cell growth under control in tissues like the colon.
🚨 Mutated APC
Most mutations are truncating (nonsense or frameshift), resulting in a nonfunctional APC protein.
This leads to:
Stabilization and accumulation of β-catenin
Constitutive activation of Wnt signaling
Overexpression of proliferation-promoting genes (e.g., MYC, CCND1)
Result: uncontrolled epithelial proliferation and early polyp formation, especially in the colon
🧬 Clinical Implications
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