TRs突变及其下游通路与肿瘤相关研究进展

信号通路是肿瘤发生、发展、预防及治疗的重要研究领域,现已公认Ras和P13K等是肿瘤发生发展的重要信号通路,甲状腺激素（TH）及其受体（TRs）可以影响这些通路起到抑制癌细胞生长和转移的作用,并逐渐成为研究的热点。近年研究发现甲状腺激素／受体影响B—catenin降解的机制,成为影响肿瘤发生发展的重要通路之一。而肿瘤普遍存在TRs突变现象,TRs突变严重影响了甲状腺激素／受体调解下游通路的功能,并成为激活下游癌基因的诱因。甲状腺激素／受体介导的B—catenin降解机制,不仅丰富了它们在抑制肿瘤发生发展中的作用机制,并进一步为突变受体对下游癌基因的持续激活提供了强有力的理论依据,最终会指导临床,将会为肿窟预防和分子靶基因治疗提供新的理论依据。

TRs mutation and downstream path of thyroid hormone/acceptor research progress in tumor

Signal path is an important domain of tumor research of development, precaution and therapeutics, Ras and PI3K path have considered to be important signal path in tumor development. Many research find that thyroid hormone（TH） and acceptor（TRs） can influence these paths and inhibit tumor development, which gradually become a hot spot of research. For the past few years, the mechanism of thyroid hormone/acceptor influencing β - catenin become an important path of influencing tumor development. However,there was a widely TRs mutation phenomenon in tumor, the mutating TRs influence the function of thyroid hormone/acceptor and become the motivation of oncogene activating. The mechanism of thyroid hormone/acceptor influencing β - catenin not only enrichs the mechanisms of thyroid hormone/aeceptor inhibiting tumor development, but also provids drastic theory for the mutating TRs becoming the motivation of oncogene activating. Along with the finding of new path,it may use and guide clinic and provide a new theory for tumor preservation and therapy.