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Clin Transl Med. 2015 Mar 7;4:11. doi: 10.1186/s40169-014-0045-y. eCollection 2015.

MELK-a conserved kinase: functions, signaling, cancer, and controversy.

Author information

1
Department of Neurological Surgery, The Ohio State University, 385 Wiseman Hall, 410 W 12th St., 43210 Columbus, OH USA.
2
Semel Institute for Psychiatry and Human Behavior and the Jonsson Comprehensive Cancer Center, UCLA School of Medicine, Columbus, USA.
3
Laboratory of Biosignaling & Therapeutics Department of Cellular and Molecular Medicine Campus Gasthuisberg, Gasthuisberg, Belgium.
4
Department of Neurological Surgery, The Ohio State University, 385 Wiseman Hall, 410 W 12th St., 43210 Columbus, OH USA ; The James Comprehensive Cancer Center, The Ohio State University, Columbus, USA.

Abstract

Maternal embryonic leucine zipper kinase (MELK) is a highly conserved serine/threonine kinase initially found to be expressed in a wide range of early embryonic cellular stages, and as a result has been implicated in embryogenesis and cell cycle control. Recent evidence has identified a broader spectrum of tissue expression pattern for this kinase than previously appreciated. MELK is expressed in several human cancers and stem cell populations. Unique spatial and temporal patterns of expression within these tissues suggest that MELK plays a prominent role in cell cycle control, cell proliferation, apoptosis, cell migration, cell renewal, embryogenesis, oncogenesis, and cancer treatment resistance and recurrence. These findings have important implications for our understanding of development, disease, and cancer therapeutics. Furthermore understanding MELK signaling may elucidate an added dimension of stem cell control.

KEYWORDS:

Cancer; Cancer therapeutics; Cancer-initiating cells; Development; Glioblastoma; Glioma-initiating cells; MELK; Maternal embryonic leucine zipper kinase; Mitotic kinase

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