受体酪氨酸激酶在 BRAF 突变癌症中的作用和功能

Receptors Pub Date : 2024-03-04 DOI:10.3390/receptors3010005
B. Biersack, L. Tahtamouni, Michael Höpfner
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引用次数: 0

摘要

强效 BRAF 抑制剂的开发彻底改变了 BRAF 突变癌症(尤其是黑色素瘤)的治疗方法。然而,其他实体的 BRAF 突变癌症,如结直肠癌,对 BRAF 抑制剂的反应明显减弱。此外,癌症对 BRAF 抑制剂治疗产生耐药性也是一个严重问题。MAPK/ERK信号的重新激活被认为是BRAF抑制剂耐药的一个重要模式。受体酪氨酸激酶(RTKs)本身就是重要的抗癌药物靶点,它们在 BRAF 抑制剂耐药性的产生、MAPK/ERK 信号转导的重新激活以及旁路信号通路的建立中起着至关重要的作用。MAPK 的重新激活可通过 RTKs 表达的增加、RTK 信号转导的改变以及翻译后过程等途径发生。本综述总结了相关 RTKs 对 BRAF 突变癌症和 BRAF 抑制剂耐药性的影响,并概述了规避 BRAF 相关耐药机制的可能和已证实的方法。
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Role and Function of Receptor Tyrosine Kinases in BRAF Mutant Cancers
The development of potent BRAF inhibitors has revolutionized the treatment of BRAF mutant cancers, in particular, melanomas. However, BRAF mutant cancers of other entities, e.g., colorectal cancers, display distinctly reduced responses to BRAF inhibitors. In addition, the emergence of cancer resistance to BRAF inhibitor treatment poses a severe problem. The reactivation of MAPK/ERK signaling was identified as an important mode of BRAF inhibitor resistance. Receptor tyrosine kinases (RTKs), which are prominent anticancer drug targets in their own right, play a crucial role in the development of drug resistance to BRAF inhibitors and the reactivation of MAPK/ERK signal transduction, as well as the establishment of bypassing signaling pathways. MAPK reactivation can occur via increased expression of RTKs, altered RTK signaling, and post-translational processes, among others. This review summarizes the influence of pertinent RTKs on BRAF mutant cancers and BRAF inhibitor resistance and outlines possible and proven ways to circumvent BRAF-associated resistance mechanisms.
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