چکیده انگلیسی:
Context: Cancer is the leading cause of death in the human population, ensuing from the accumulation of damage to genetic materials and affecting various parts of the organs. This review is focused on the cell signaling cross-talk mechanism of colorectal cancer (CRC) and its regulations. Genomic instability acts as the major driving force for CRC. The major CRC cascade mechanisms such as Wnt, Ras, TOPK, p53, and ubiquitin pathways were discussed. These interlinked signals cross-talk with one another in various regulatory mechanisms and play a unique role in CRC. Evidence Acquisition: The major cross-talking signals of CRC are the most significant part of this review. Wnt is a resource and center of axis for cross-talk and interlinked signaling mechanism. Wnt/β-catenin signaling was regulated by frizzled receptor, co-factors, Ras, TOPK, and many other mechanisms; related literature of CRC were collected through a literature survey and categorized using the keywords. The pathways with high specificity interlinked with Wnt were identified and used as the major targets for this review. Results and Conclusion: The interlinked signaling pathways and gene networks were explained with their specificity role in CRC. We highlighted the major regulatory signaling and interlinked pathways of CRC, as new multi targets approach. Furthermore, we discussed the potent targeted genes, bio-markers for a better prognosis, and therapies for CRC patients. Through highlighting the gene cross-talking signaling cascade; we have provided the source for gene network interaction and targeted therapy. This study paves the way for multi-targeting of interlinked pathways and suggesting these would be perfect for suppressing of CRC. The signaling pathways discussed in this review are not only focused on CRC but also the new potent targets and bio-markers for different types of cancers. Targeting multiple interlinked pathways could be useful for developing new potential bio-markers for treatment and diagnosis purposes.
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