RESUMEN
Sporadic colorectal cancer (CRC) is strongly linked to extraneous factors, like poor diet and lifestyle, but not to inherent factors like familial genetics. The changes at the epigenomics and signalling pathways are known across the sporadic CRC stages. The catch is that temporal information of the onset, the feedback loop, and the crosstalk of signalling and noise are still unclear. This makes it challenging to diagnose and treat colon cancer effectively with no relapse. Various microbial cells and native cells of the colon, contribute to sporadic CRC development. These cells secrete autocrine and paracrine for their bioenergetics and communications with other cell types. Imbalances of the biochemicals affect the epithelial lining of colon. One side of this epithelial lining is interfacing the dense colon tissue, while the other side is exposed to microbiota and excrement from the lumen. Hence, the epithelial lining is prone to tumorigenesis due to the influence of both biochemical and mechanical cues from its complex surrounding. The role of physical transformations in tumorigenesis have been limitedly discussed. In this context, cellular and tissue structures, and force transductions are heavily regulated by cell adhesion networks. These networks include cell anchoring mechanism to the surrounding, cell structural integrity mechanism, and cell effector molecules. This review will focus on the progression of the sporadic CRC stages that are governed by the underlaying cell adhesion networks within the epithelial cells. Additionally, current and potential technologies and therapeutics that target cell adhesion networks for treatments of sporadic CRC will be incorporated.
