ERK5信号在结直肠癌中的作用

K. Taniguchi, P. R. D. Jong
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引用次数: 0

摘要

丝裂原活化蛋白激酶(MAPK)家族包括ERK1/2、p38、JNK和ERK5。MAPKs在结直肠癌(CRC)中的作用是明确的,特别是ERK1/2。受体酪氨酸激酶的异常激活或关键上游转导(包括KRAS和BRAF)的功能获得突变是mapk介导的结直肠癌肿瘤进展的原因。与ERK1/2相比,ERK5在结直肠癌发展中的作用被低估了。在这里,我们讨论了ERK5信号参与CRC发生和进展的最新证据,以及它在靶向治疗耐药中的假定作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of ERK5 signaling in colorectal cancer
The mitogen-activated protein kinase (MAPK) family includes ERK1/2, p38, JNK and ERK5. The role of MAPKs in colorectal cancer (CRC) is well-established, in particular ERK1/2. Abnormal activation of receptor tyrosine kinases or gain-of-function mutations in critical upstream transducers, including KRAS and BRAF, are responsible for MAPK-mediated tumor progression in CRC. Compared to ERK1/2, the role of ERK5 in CRC development has been underrated. Here we discuss recent evidence for the involvement of ERK5 signaling in the development and progression of CRC, as well as its putative role in resistance to targeted therapy.
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