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Cancers 2016, 8(5), 51;

MLK3 Signaling in Cancer Invasion

Cell and Molecular Biology program, Michigan State University, East Lansing, MI 48824, USA
Department of Physiology, Michigan State University, East Lansing, MI 48824, USA
Author to whom correspondence should be addressed.
Academic Editor: Vita Golubovskaya
Received: 13 April 2016 / Revised: 5 May 2016 / Accepted: 10 May 2016 / Published: 19 May 2016
(This article belongs to the Special Issue Cancer Cell Invasion)
Full-Text   |   PDF [1739 KB, uploaded 19 May 2016]   |  


Mixed-lineage kinase 3 (MLK3) was first cloned in 1994; however, only in the past decade has MLK3 become recognized as a player in oncogenic signaling. MLK3 is a mitogen-activated protein kinase kinase kinase (MAP3K) that mediates signals from several cell surface receptors including receptor tyrosine kinases (RTKs), chemokine receptors, and cytokine receptors. Once activated, MLK3 transduces signals to multiple downstream pathways, primarily to c-Jun terminal kinase (JNK) MAPK, as well as to extracellular-signal-regulated kinase (ERK) MAPK, P38 MAPK, and NF-κB, resulting in both transcriptional and post-translational regulation of multiple effector proteins. In several types of cancer, MLK3 signaling is implicated in promoting cell proliferation, as well as driving cell migration, invasion and metastasis. View Full-Text
Keywords: cancer invasion; signal transduction; mixed lineage kinase 3 (MLK3); metastasis cancer invasion; signal transduction; mixed lineage kinase 3 (MLK3); metastasis

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Rattanasinchai, C.; Gallo, K.A. MLK3 Signaling in Cancer Invasion. Cancers 2016, 8, 51.

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