结直肠癌的调控途径及其协同串扰机制

M. Jothimani, L. Loganathan, Prahashini Palanisamy, K. Muthusamy
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引用次数: 2

摘要

背景:癌症是人类死亡的主要原因,是由于遗传物质损伤的积累和影响到器官的各个部分。本文就结直肠癌(CRC)的细胞信号串扰机制及其调控作一综述。基因组不稳定性是结直肠癌的主要驱动因素。讨论了Wnt、Ras、TOPK、p53和泛素通路等CRC的主要级联机制。这些相互关联的信号在各种调控机制中相互串扰,在CRC中发挥着独特的作用。证据获取:CRC的主要串扰信号是本综述最重要的部分。Wnt是串扰和互联信号机制的资源和轴心。Wnt/β-catenin信号受卷曲受体、辅助因子、Ras、TOPK等多种机制调控;通过文献调查收集结直肠癌的相关文献,并用关键词进行分类。确定了与Wnt相关的高特异性通路,并将其作为本综述的主要靶点。结果与结论:在结直肠癌中解释了相互关联的信号通路和基因网络及其特异性作用。我们强调了CRC的主要调控信号和相互关联的途径,作为新的多靶点方法。此外,我们讨论了有效的靶向基因,生物标志物,为更好的预后和治疗结直肠癌患者。通过强调基因串扰信号级联;我们为基因网络相互作用和靶向治疗提供了来源。这项研究为多靶向相互关联的通路铺平了道路,并表明这些通路将是抑制结直肠癌的完美途径。本文不仅对结直肠癌的信号通路进行了综述,还对不同类型癌症的新的有效靶点和生物标志物进行了综述。靶向多个相互关联的通路可能有助于开发用于治疗和诊断目的的新的潜在生物标志物。
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Regulatory pathways of colorectal cancer and their synergistic cross-talk mechanism
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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