# CTNNA2

Source: https://onco.cc/targets/ctnna2/  
OnCo record `ctnna2` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

CTNNA2 (Catenin alpha-2) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver and a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Prostate cancer, Hepatocellular carcinoma, Head and neck squamous cell carcinoma and 4 more.

## Summary

May function as a linker between cadherin adhesion receptors and the cytoskeleton to regulate cell-cell adhesion and differentiation in the nervous system. Required for proper regulation of cortical neuronal migration and neurite growth. It acts as a negative regulator of Arp2/3 complex activity and Arp2/3-mediated actin polymerisation.

IntOGen calls it a driver in 12 cohorts (9 activating, 2 loss-of-function), covering Cholangiocarcinoma, Hepatocellular Carcinoma, Head and Neck Squamous Cell Carcinoma, Lung Adenocarcinoma, Melanoma, Pancreatic Adenocarcinoma and others.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: catenin alpha 2; Catenin alpha-2; CAP-R; CT114
- Tags: cancer-genes-wave
- Symbol: CTNNA2
- Class: oncogene
- Biology: May function as a linker between cadherin adhesion receptors and the cytoskeleton to regulate cell-cell adhesion and differentiation in the nervous system. Required for proper regulation of cortical neuronal migration and neurite growth. It acts as a negative regulator of Arp2/3 complex activity and Arp2/3-mediated actin polymerisation. It thereby suppresses excessive actin branching which would impair neurite growth and stability. Regulates morphological plasticity of synapses and cerebellar and hippocampal lamination during development. Functions in the control of startle modulation. Location: Cell membrane; Cytoplasm; Cytoplasm, cytoskeleton; Cell junction, adherens junction (UniProt). Locus 2p12 (HGNC).
- Where found: Prostate cancer: IntOGen driver in 4 cohorts (PRAD); Hepatocellular carcinoma: IntOGen driver in 1 cohort (HCC); Head and neck squamous cell carcinoma: IntOGen driver in 1 cohort (HNSC); Pancreatic ductal adenocarcinoma: IntOGen driver in 1 cohort (PAAD); Biliary tract cancer: IntOGen driver in 2 cohorts (CHOL); Non-small-cell lung cancer: IntOGen driver in 2 cohorts (LUAD)

## Notes

- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: IntOGen calls it an activating (Act) driver in 9 cohorts; IntOGen calls it a loss-of-function (LoF) driver in 2 cohorts. Evidence tier "cohort-driver" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.

## Sources

- HGNC HGNC:2510: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:2510
- UniProt P26232: https://www.uniprot.org/uniprotkb/P26232/entry
- NCBI Gene 1496: https://www.ncbi.nlm.nih.gov/gene/1496
- Ensembl ENSG00000066032: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000066032

## Connected records

- collections: [IntOGen](https://onco.cc/collections/intogen/)
- cancers: [Biliary tract cancer (cholangiocarcinoma)](https://onco.cc/cancers/cholangiocarcinoma/), [Head and neck squamous cell carcinoma](https://onco.cc/cancers/head-and-neck/), [Hepatocellular carcinoma](https://onco.cc/cancers/hcc/), [Melanoma](https://onco.cc/cancers/melanoma/), [Non-small-cell lung cancer](https://onco.cc/cancers/nsclc/), [Pancreatic ductal adenocarcinoma](https://onco.cc/cancers/pancreatic/), [Prostate cancer](https://onco.cc/cancers/prostate/)

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JSON: https://onco.cc/api/v1/entities/ctnna2.json