Abstract
Maternal embryonic leucine zipper kinase (MELK) functions as a modulator of intracellular signaling and affects various cellular and biological processes, including cell cycle, cell proliferation, apoptosis, spliceosome assembly, gene expression, embryonic development, hematopoiesis, and oncogenesis. In these cellular processes, MELK functions by binding to numerous proteins. In general, the effects of multiple protein interactions with MELK are oncogenic in nature, and the overexpression of MELK in kinds of cancer provides some evidence that it may be involved in tumorigenic process. In this review, our current knowledge of MELK function and recent discoveries in MELK signaling pathway were discussed. The regulation of MELK in cancers and its potential as a therapeutic target were also described.
Highlights
According to studies on oncogenic signal transduction pathways, targeted therapies have made great progress in cancer treatment, whereas standard chemotherapy alone has failed to improve treatment outcome
It is reported that PIG-1 and cell death gene-3 (CED-3) double mutants result in nearly 100% of lineages producing extra HSN and PHB neurons, leading to dramatically stronger programmed cell death than either single mutant, which suggests that PIG-1 acts at least partly in parallel to the canonical cell death pathway [21]
Preliminary evidence has indicated that Maternal embryonic leucine zipper kinase (MELK) is involved in various cellular processes by binding to numerous proteins, thereby resulting in cell cycle regulation, cell proliferation, apoptosis, spliceosome assembly, gene expression, hematopoiesis, embryonic development, and oncogenesis [12,13,36,40,49,50]
Summary
According to studies on oncogenic signal transduction pathways, targeted therapies have made great progress in cancer treatment, whereas standard chemotherapy alone has failed to improve treatment outcome. Maternal embryonic leucine zipper kinase (MELK), a potential therapeutic target that is possibly involved in a tumorigenic process, was described. MELK is a cell cycle-dependent protein kinase that belongs to the KIN1/PAR-1/MARK family [2,4,5]. Unlike most members of this family only functioning in cell survival under metabolically challenging conditions [6,7,8,9], MELK participates in diverse processes, including cell cycle [4], cell proliferation [10], apoptosis [11,12], RNA processing [13], and embryonic development [3,14,15,16]. MELK is involved in multiple protein interactions that affect many stages of tumorigenesis [17]. This gene is potentially an effective therapeutic target
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