Abstract
RNA-binding proteins may regulate every aspect of RNA metabolism, including pre-mRNA splicing, mRNA trafficking, stability and translation of many genes. The dynamic association of these proteins with RNA defines the lifetime, cellular localization, processing and the rate at which a specific mRNA is translated. One of the pathways involved in regulating of mRNA stability is mediated by adenylate uridylate-rich element (ARE) binding proteins. These proteins are involved in processes of apoptosis, tumorigenesis and development. Out of many ARE-binding proteins, two of them AUF1 and HuR were studied most extensively and reported to regulate the mRNA stability in vivo. Our previously published data demonstrate that both proteins are involved in thyroid carcinogenesis. Several other reports postulate that mRNA binding proteins may participate in thyroid hormone actions. However, until now, exacts mechanisms and the possible role of post-transcriptional regulation and especially the role of AUF1 and HuR in those processes remain not fully understood. In this study we shortly review the possible function of both proteins in relation to development and various physiological and pathophysiological processes, including thyroid function and disorders.
Highlights
Cytoplasmic stability of eukaryotic mRNA is a substantially important check point in the control for gene expression
A common feature of many unstable mRNAs is the presence of an Adenylate-Uridylate-rich element (ARE) within the 3’-untranslated region (3’-UTR) [1,2,3]
We demonstrated that down-regulation of CD9, CD82 and RKIP may reflect an increased in vivo metastatic potential of thyroid cancer cells [56,57]
Summary
Cytoplasmic stability of eukaryotic mRNA is a substantially important check point in the control for gene expression. It is worth to note that HuR was able to interact with several transcription factors crucial for proper morphogenesis, patterning and specification, and for thyroid development such as Hox-A5 [29].The absence of Hox-A5 is related to disorganized follicle formation; decreased TPO; Nkx2.1, Titf, altered Pax gene expression, but normal serum T4 level. As demonstrated, these mRNAs bear AREsequences and are crucial for thyroid development (Table 2). Such a cytoplasmic-nuclear translocation of AUF1 allowed the cells initiation of differentiation followed by induction of milk production and inhibition of proliferation [84]
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