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Protein / target

Adenomatous polyposis coli protein

Encoded byAPCP25054Homo sapiensSwiss-Prot
UniProt: P25054Ensembl: ENSG00000134982HGNC: HGNC:583NCBI Gene: 324
Small-molecule tractable
Druggability
Structure with Ligand
1
Research papers

Protein at a glance

Biological role

Protein kinase regulator

Strongest disease association

Adenomatous Polyposis Coli

Via encoding gene APC · Genetic evidence · score 0.96

Research activity

Emerging research

1 papers · latest 2020

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Tumor suppressor.

View complete UniProt function annotation

Tumor suppressor. Promotes rapid degradation of CTNNB1 and participates in Wnt signaling as a negative regulator. APC activity is correlated with its phosphorylation state. Activates the GEF activity of SPATA13 and ARHGEF4. Plays a role in hepatocyte growth factor (HGF)-induced cell migration. Required for MMP9 up-regulation via the JNK signaling pathway in colorectal tumor cells. Associates with both microtubules and actin filaments, components of the cytoskeleton (PubMed:17293347). Plays a role in mediating the organization of F-actin into ordered bundles (PubMed:17293347). Functions downstream of Rho GTPases and DIAPH1 to selectively stabilize microtubules (By similarity). Acts as a mediator of ERBB2-dependent stabilization of microtubules at the cell cortex. It is required for the localization of MACF1 to the cell membrane and this localization of MACF1 is critical for its function in microtubule stabilization

Subcellular location

Cell junction, adherens junctionCytoplasm, cytoskeletonCell projection, lamellipodiumCell projection, ruffle membraneCytoplasmCell membrane
Domains and Gene Ontology detail (55)

Gene Ontology

  • Cadherens junction
  • Cbeta-catenin destruction complex
  • Cbicellular tight junction
  • Ccatenin complex
  • Ccentrosome
  • Ccytoplasm
  • Ccytosol
  • Ckinetochore
  • Clamellipodium
  • Clateral plasma membrane
  • Cmicrotubule
  • Cnucleoplasm

2843 aa · 312 kDa · 3 isoforms

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Cell migrationUniProt · GOReceptor tyrosine kinase signallingUniProtCell proliferation & survivalGOCell-cycle regulationGOCell adhesionUniProt · GO
View supporting evidence

Cell migration

  • ·Tumor suppressor. Promotes rapid degradation of CTNNB1 and participates in Wnt signaling…
  • ·cell migration
  • ·positive regulation of cell migration

Receptor tyrosine kinase signalling

  • ·Tumor suppressor. Promotes rapid degradation of CTNNB1 and participates in Wnt signaling…

Cell proliferation & survival

  • ·negative regulation of cell population proliferation

Cell-cycle regulation

  • ·negative regulation of G1/S transition of mitotic cell cycle

Cell adhesion

  • ·Cell junction, adherens junction
  • ·bicellular tight junction
  • ·bicellular tight junction assembly
  • ·cell adhesion

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene APC

Gene-level evidence surfaced through the gene APCthat encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Adenomatous Polyposis Coli
0.98Well supported

Genetic evidence dominant · Open Targets 0.78

Carcinoma, Hepatocellular
0.97Well supported

Genetic evidence dominant · Open Targets 0.71

Colonic Neoplasms
0.94Well supported

Genetic evidence dominant · Open Targets 0.72

Colon carcinoma
0.93Well supported

Genetic evidence dominant · Open Targets 0.73

Colorectal Neoplasms
0.90Well supported

Genetic evidence dominant · Open Targets 0.72

View evidence synthesis (5)
Adenomatous Polyposis ColiWell supported
0.98
agreement 0.86–1.00
Genetic67%Animal model24%Literature10%Genetic literaturedup

Open Targets aggregate 0.78 · 3 independent evidence families · 1 not counted as duplicate

Carcinoma, HepatocellularWell supported
0.97
agreement 0.87–1.00
Genetic54%Somatic mutation20%Animal model18%Literature8%Genetic literaturedup

Open Targets aggregate 0.71 · 4 independent evidence families · 1 not counted as duplicate

Colonic NeoplasmsWell supported
0.94
agreement 0.82–1.00
Genetic62%Somatic mutation28%Literature10%

Open Targets aggregate 0.72 · 3 independent evidence families

Colon carcinomaWell supported
0.93
agreement 0.82–1.00
Genetic69%Somatic mutation27%Literature4%

Open Targets aggregate 0.73 · 3 independent evidence families

Colorectal NeoplasmsWell supported
0.90
agreement 0.78–1.00
Genetic66%Animal model24%Literature11%Genetic literaturedup

Open Targets aggregate 0.72 · 3 independent evidence families · 1 not counted as duplicate

The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations
Adenomatous Polyposis Coli0.78
Colon carcinoma0.73
Colorectal adenocarcinoma0.73
Colorectal Neoplasms0.72
Colonic Neoplasms0.72
Carcinoma, Hepatocellular0.71
Desmoid Tumors0.70

Tractability

Small molecules — Emerging

Feasibility evidence (structure with ligand and high-quality ligand) — no clinical-stage drug of this modality recorded.

Antibodies — Emerging

Feasibility evidence (uniprot loc high conf and go cc high conf) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

Feasibility evidence (uniprot ubiquitination and database ubiquitination) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (9)
SM · Structure with LigandSM · High-Quality LigandAB · UniProt loc high confAB · GO CC high confAB · Human Protein Atlas locPR · UniProt UbiquitinationPR · Database UbiquitinationPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2020

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

Molecular Mechanisms of Colon Cancer Progression and Metastasis: Recent Insights and Advancements.261 cites

Malki A · International journal of molecular sciences · 2020

Recent

Molecular Mechanisms of Colon Cancer Progression and Metastasis: Recent Insights and Advancements.

Malki A · International journal of molecular sciences · 2020

Europe PMC papers linked directly to this protein.