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APC gene
URL of this page: https://medlineplus.gov/genetics/gene/apc/

APC gene

APC regulator of Wnt signaling pathway

Normal Function

The APC gene provides instructions for making the APC protein, which plays a critical role in several cellular processes. The APC protein acts as a tumor suppressor, which means that it keeps cells from growing and dividing too fast or in an uncontrolled way. This protein blocks a chemical signaling pathway known as Wnt signaling. This pathway promotes cell growth and division (proliferation) and controls the activity (expression) of certain genes. 

The APC protein attaches (binds) to multiple proteins to form a complex that helps to control levels of another protein called beta-catenin. Beta-catenin is a key part of the Wnt pathway, and it helps control many cell functions, including cell proliferation, gene expression, and the process by which cells mature to carry out specific functions (differentiation). When the APC protein complex binds beta-catenin, it helps break the protein down when it is no longer needed.

The APC protein also plays a role in regulating cell division. The protein interacts with parts of the cell's structural framework (cytoskeleton) to help with proper cell organization during cell division. This helps ensure that the number of chromosomes in a cell is correct after the cell divides. 


Health Conditions Related to Genetic Changes

Desmoid tumor

Variants (also called mutations) in the APC gene have been found in people with a type of aggressive but noncancerous (benign) growth called a desmoid tumor. These rare tumors arise from connective tissue, which provides strength and flexibility to structures such as bones, ligaments, and muscles.

In people with APC gene variants, desmoid tumors are associated with a condition called familial adenomatous polyposis (FAP, described below) that greatly increases the risk of cancer of the large intestine (colon) and rectum (collectively known as colorectal cancer). People with FAP have a risk of developing a desmoid tumor that is 800 times greater the risk among the general population.

Desmoid tumors most commonly occur in the abdomen or abdominal wall, but these tumors can also occur in other parts of the body. APC gene variants are found in about 10 percent of people with desmoid tumors.

Most of the APC gene variants that are associated with FAP and desmoid tumors cause cells to produce an abnormally short version of the APC protein. The shortened protein is unable to help break down beta-catenin when it is no longer needed. Excess beta-catenin promotes uncontrolled growth and division of cells, which causes FAP and predisposes individuals to develop a desmoid tumor.

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Familial adenomatous polyposis

Hundreds of different variants in the APC gene have been found to cause familial adenomatous polyposis (FAP). This condition is characterized by multiple precancerous growths (polyps) in the colon. One or more of these polyps can develop into cancer of the colon and rectum (together known as colorectal cancer) if the polpys are not removed. Ten to 30 percent of people with FAP develop a desmoid tumor.

Most of the APC gene variants that cause FAP lead to the production of an abnormally short, nonfunctional version of the APC protein. This shortened protein prevents the complex from binding to beta-catenin when it is no longer needed and breaking it down. The excess beta-catenin allows the Wnt chemical signaling pathway to stay active, which can lead to uncontrolled cell growth. This leads to the formation of polyps in the colon, which can become cancerous. Additionally, the nonfunctional APC protein can impair normal cell division, which may contribute to cancer development in people with FAP.

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Primary macronodular adrenal hyperplasia

MedlinePlus Genetics provides information about Primary macronodular adrenal hyperplasia

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Other cancers

Variants that affect the APC gene have been found to cause a condition called gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS). People with GAPPS can have hundreds of polyps that develop in the stomach, which increases the risk of stomach (gastric) cancer. In these cases, the cancer is limited to the stomach without spreading to the colon or other structures in the digestive tract.

The gene variants that cause GAPPS occur in an area near the APC gene called the promoter region, which controls the production of the APC protein. These variants impair the function of the promoter region and reduce the expression of the APC gene. 

Other Names for This Gene

  • adenomatous polyposis coli
  • APC_HUMAN
  • WNT signaling pathway regulator

Additional Information & Resources

Tests Listed in the Genetic Testing Registry

Scientific Articles on PubMed

Catalog of Genes and Diseases from OMIM

Gene and Variant Databases

References

  • Abbott J, Nathke IS. The adenomatous polyposis coli protein 30 years on. Semin Cell Dev Biol. 2023 Dec;150-151:28-34. doi: 10.1016/j.semcdb.2023.04.004. Epub 2023 Apr 22. Citation on PubMed
  • Ditonno I, Novielli D, Celiberto F, Rizzi S, Rendina M, Ierardi E, Di Leo A, Losurdo G. Molecular Pathways of Carcinogenesis in Familial Adenomatous Polyposis. Int J Mol Sci. 2023 Mar 16;24(6):5687. doi: 10.3390/ijms24065687. Citation on PubMed
  • Jaiswal AS, Balusu R, Narayan S. Involvement of adenomatous polyposis coli in colorectal tumorigenesis. Front Biosci. 2005 May 1;10:1118-34. doi: 10.2741/1605. Citation on PubMed
  • Joo JE, Viana-Errasti J, Buchanan DD, Valle L. Genetics, genomics and clinical features of adenomatous polyposis. Fam Cancer. 2025 Apr 16;24(2):38. doi: 10.1007/s10689-025-00460-0. Citation on PubMed
  • Lips DJ, Barker N, Clevers H, Hennipman A. The role of APC and beta-catenin in the aetiology of aggressive fibromatosis (desmoid tumors). Eur J Surg Oncol. 2009 Jan;35(1):3-10. doi: 10.1016/j.ejso.2008.07.003. Epub 2008 Aug 21. Citation on PubMed
  • Sena P, Saviano M, Monni S, Losi L, Roncucci L, Marzona L, De Pol A. Subcellular localization of beta-catenin and APC proteins in colorectal preneoplastic and neoplastic lesions. Cancer Lett. 2006 Sep 28;241(2):203-12. doi: 10.1016/j.canlet.2005.10.011. Epub 2005 Nov 17. Citation on PubMed
  • Senda T, Shimomura A, Iizuka-Kogo A. Adenomatous polyposis coli (Apc) tumor suppressor gene as a multifunctional gene. Anat Sci Int. 2005 Sep;80(3):121-31. doi: 10.1111/j.1447-073x.2005.00106.x. Citation on PubMed
  • Tejpar S, Michils G, Denys H, Van Dam K, Nik SA, Jadidizadeh A, Cassiman JJ. Analysis of Wnt/Beta catenin signalling in desmoid tumors. Acta Gastroenterol Belg. 2005 Jan-Mar;68(1):5-9. Citation on PubMed
  • Yang W, Ding PR. Update on Familial Adenomatous Polyposis-Associated Desmoid Tumors. Clin Colon Rectal Surg. 2023 Apr 17;36(6):400-405. doi: 10.1055/s-0043-1767709. eCollection 2023 Nov. Citation on PubMed
  • Yen T, Stanich PP, Axell L, Patel SG. APC-Associated Polyposis Conditions. 1998 Dec 18 [updated 2022 May 12]. In: Adam MP, Feldman J, Mirzaa GM, Pagon RA, Wallace SE, Amemiya A, editors. GeneReviews(R) [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2025. Available from http://www.ncbi.nlm.nih.gov/books/NBK1345/ Citation on PubMed

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