Adenomatous polyposis coli (APC) is widely recognized as a heavily mutated gene that suppresses tumor growth in colorectal cancer (CRC). Its mutation is considered to be the primary and early event that occurs in the development of CRC. In addition, APC has a crucial role in inhibiting the canonical Wnt signaling pathway. APC mutations in CRC result in the production of shortened gene products. This impairment of β-catenin destruction complexes causes an accumulation of active β-catenin in the cytoplasm and nucleus. In these compartments, β-catenin can bind with DNA-binding proteins of the transcription factor/lymphoid enhancer-binding factor family, thereby activating the Wnt signaling pathway. Consequently, the balance of numerous cellular processes is disrupted, ultimately driving the formation of tumors. There is a growing body of evidence indicating the prevalent occurrence of APC truncation in the majority of CRC cases. Furthermore, it has been observed that these truncated proteins have a crucial role in the activation of the Wnt signaling pathway and the subsequent loss of tumor inhibitory function. This review aimed to provide an overview of the recent advancements in understanding the mechanism behind APC truncation and its association with the onset and progression of CRC.
Keywords: APC truncation; Wnt signaling pathway; adenomatous polyposis coli; colorectal cancer; tumor growth; tumorigenesis.
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