Abstract
Powerful bioinformatics tools have provided a wealth of novel miRNA–transcription factor networks crucial in controlling gene regulation. In this review, we focus on the biological functions of miRNAs targeting ZNF521, explaining the molecular mechanisms by which the dysregulation of this axis contributes to malignancy. ZNF521 is a stem cell-associated co-transcription factor implicated in the regulation of hematopoietic, neural, and mesenchymal stem cells. The aberrant expression of ZNF521 transcripts, frequently associated with miRNA deregulation, has been detected in several tumors including pancreatic, hepatocellular, gastric, bladder transitional cell carcinomas as well as in breast and ovarian cancers. miRNA expression profiling tools are currently identifying a multitude of miRNAs, involved together with oncogenes and TFs in the regulation of oncogenesis, including ZNF521, which may be candidates for diagnostic and prognostic biomarkers of cancer.
Highlights
The Complex Regulatory Network between miRNAs and Transcription FactorsMost of the miRNA targets are transcription factors (TFs), which are critical in transregulating gene networks in many cellular systems [1]
The miRNA–transcription factors (TFs) target regulation is orchestrated by a complex mechanism in which the expression of a miRNA can be regulated by TFs, and a gene encoding TFs can be inhibited by miRNAs [7] (Figure 1)
ZNF521 protein was initially two models: in feed forward loops (FFLs) working in a miRNA-mediated manner, the miRNA may simultaidentified for its abundant expression in hematopoietic stem/progenitor cells and its levels neously repress the TF and its target genes; in TF-mediated FFLs, a TF is able are progressively reduced during myeloid differentiation [13]
Summary
Most of the miRNA targets are transcription factors (TFs), which are critical in transregulating gene networks in many cellular systems [1]. ZNF521 protein was initially two models: in FFLs working in a miRNA-mediated manner, the miRNA may simultaidentified for its abundant expression in hematopoietic stem/progenitor cells and its levels neously repress the TF and its target genes; in TF-mediated FFLs, a TF is able are progressively reduced during myeloid differentiation [13]. In addition to the role for ZNF521 in cell fate determination in different types of progenitor cells, this TF plays a crucial role in cancer malignancies The overexpression of this protein sustains clonogenic growth, migration and tumorigenicity of medulloblastoma cells, and recently it was demonstrated to interact with GLI1 and GLI2 proteins stimulating the trans-activation of the Sonic Hedgehog pathway in medulloblastoma [25,26].
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