Roles Each of Snail, Yin Yang 1 and RKIP in the Regulation of Tumor Cells Chemo-immuno-resistance to Apoptosis.
Roles Each of Snail, Yin Yang 1 and RKIP in the Regulation of Tumor Cells Chemo-immuno-resistance to Apoptosis.
复制标题
DOI：
10.1615/forumimmundisther.2013008299
复制
发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Baritaki S
中科院分区：
文献类型：
--
作者：
Bonavida B;Jazirehi A;Vega MI;Huerta-Yepez S;Baritaki S
目前的抗癌治疗体系包括手术、化疗、放疗、激素治疗、免疫治疗及其联合治疗。初始治疗通常会导致客观的临床反应，并延长大部分治疗患者的总生存期（OS）和无进展生存期（PFS）。然而，在发病时，有一部分患者没有反应，另一部分患者最初有反应，但经历了复发和复发。后一类患者对各种不相关的治疗产生交叉耐药状态。因此，迫切需要首先揭示抗性的潜在机制和调控交叉抗性的相关基因产物。这些基因产物是潜在的治疗靶点以及潜在的预后/诊断生物标志物。在这种情况下，我们已经确定了涉及耐药的三个相关基因产物，即Snail， YY1和RKIP，它们是许多癌症中失调的NF-κB/Snail/YY1/RKIP环的组成部分。在这篇综述中，我们将讨论Snail， YY1和RKIP在调节肿瘤细胞对化疗和免疫治疗的耐药性中的作用。由于这些相同的基因产物也被证明参与了EMT表型和转移的调控，我们建议靶向这三个基因产物中的任何一个都可以同时抑制肿瘤细胞的抵抗和转移。
The current anti-cancer therapeutic armamentarium consists of surgery, chemotherapy, radiation, hormonal therapy, immunotherapy, and combinations thereof. Initial treatments usually result in objective clinical responses with prolongation of overall survival (OS) and progression-free survival (PFS) in a large subset of the treated patients. However, at the onset, there is a subset of patients who does not respond and another subset that initially responded but experiences relapses and recurrences. These latter subsets of patients develop a state of cross-resistance to a variety of unrelated therapies. Therefore, there is an urgent need to first unravel the underlying mechanisms of resistance and associated gene products that regulate the cross-resistance. Such gene products are potential therapeutic targets as well as potential prognostic/diagnostic biomarkers. In this context, we have identified three interrelated gene products involved in resistance, namely, Snail, YY1, and RKIP that are components of the dysregulated NF-κB/Snail/YY1/RKIP loop in many cancers. In this review, we will discuss the roles each of Snail, YY1 and RKIP in the regulation of tumor cell resistance to chemo and immunotherapies. Since these same gene products have also been shown to be involved in the regulation of the EMT phenotype and metastasis, we suggest that targeting any of these three gene products can simultaneously inhibit tumor cell resistance and metastasis.