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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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A 2016 study studied this question.
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