Apc, short for Adenomatous Polyposis Coli, is a well-known tumor suppressor gene. It regulates the Wnt signal transduction pathway and is also an important cytoskeletal protein. Mutations in the Apc gene are closely associated with colorectal cancer and some neurological disorders. Its function is crucial in maintaining normal cell growth, adhesion, and migration, and it participates in key biological processes like cell cycle regulation [1,2].

Mutations in the Apc gene play a rate-limiting role in the majority of sporadic colorectal cancers. Loss of Apc function triggers a series of molecular and histological changes following the 'adenoma-carcinoma' sequence. Inactivation of Apc seems to endow cells with a selective advantage for clonal expansion and genetic instability for tumor progression, likely through the constitutive activation of the Wnt pathway. Additionally, Apc mutation is correlated with a poor response to immunotherapy in colon cancer, associated with lower tumor mutation burden, lower expression of immune checkpoint molecules, and less immune cell infiltration [1,3].

In conclusion, Apc is essential for normal cellular function, especially in preventing colorectal cancer. Studies on Apc, including those using gene knockout or conditional knockout mouse models (although not explicitly detailed in the provided references), have significantly contributed to our understanding of the molecular mechanisms underlying colorectal cancer development and the response to immunotherapy.

References:

1. Fodde, R. . The APC gene in colorectal cancer. In European journal of cancer (Oxford, England : 1990), 38, 867-71. doi:. https://pubmed.ncbi.nlm.nih.gov/11978510/

2. Fang, Xingyuan, Svitkina, Tatyana M. 2022. Adenomatous Polyposis Coli (APC) in cell migration. In European journal of cell biology, 101, 151228. doi:10.1016/j.ejcb.2022.151228. https://pubmed.ncbi.nlm.nih.gov/35483122/

3. Li, Bing, Zhang, Guoliang, Xu, Xuejie. 2023. APC mutation correlated with poor response of immunotherapy in colon cancer. In BMC gastroenterology, 23, 95. doi:10.1186/s12876-023-02725-3. https://pubmed.ncbi.nlm.nih.gov/36977982/