Approximately 80% of colon tumors show a loss in adenomatous polyposis coli (APC) function because of mutations that lead to the deactivation of the APC gene. The APC gene serves as a central gatekeeper gene in colon cancer. APC is crucial in the Wnt signaling pathway as well as the regulation of ?-catenin which is causes an amassing of ?-catenin in the cytoplasm and its possible translocation into the core to go about as a transcriptional coactivator of translation factors that have a place with the TCF/LEF family. Without Wnt, ?-catenin would not aggregate in the cytoplasm since a decimation complex would ordinarily degrade it. . The unquestioned tumor suppressor function of APC occurs through the formation of a compound that destroys cancerous cells. This complex is formed by the combination of APC with Axin/Axin2 and GSK-3? (Eshghifar, Farrokhi, Naji, & Zali, 2017). When a Wnt signal is lacking, the complex plays a vital role in the ubiquitination and consequent proteasomal breakdown of the oncogene ?-catenin. Consequently, the loss of APC function causes a buildup of ?-catenin, which moves to the nucleus and involves the Tcf/Lef transcription factor composite to trigger the transcription of numerous recipient genes such as c-myc, cyclinD1, and CRD-BP (Eshghifar et al., 2017). The upshots of uncontrolled ?-catenin activity with respect to tumorigenesis is linked to the direct prompting of cellular growth and propagation in addition to the disturbance of differentiation schedules (Cai, Maitra, Anders, Taketo, & Pan, 2015).Another role of APC is the promotion of microtubule stability in several cellular contexts. Nevertheless, the magnitude of the impact of interfering with this role in tumor development is unclear. Studies have reported that stabilized ?-catenin is sufficient to instigate intestinal polyposis in mice thereby indicating that interfering with microtubule-binding functions of APC is not a prerequisite for early tumorigenesis (Cai et al., 2015). In the investigations, it was shown that mice homozygous for the 1638T APC allele devoid of the microtubule- and EB1-binding areas of APC did not develop tumors. However, the ?-catenin binding domains of the mice were intact. The findings of the investigation led to the conclusion that interfering with the microtubule functions of APC influences tumor advancement rather than tumor induction. Chromosomal deletions that affect the DCC and p53 genes have also been implicated in the deactivation of tumor suppressor genes, which leads to the development of colon tumors.