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Cancers 2016, 8(5), 51; doi:10.3390/cancers8050051

MLK3 Signaling in Cancer Invasion

1
Cell and Molecular Biology program, Michigan State University, East Lansing, MI 48824, USA
2
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)
View Full-Text   |   Download PDF [1739 KB, uploaded 19 May 2016]   |  

Abstract

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
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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

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