Abstract
The human embryonic lethal abnormal vision-like protein, HuR, is a member of the Hu family of RNA-binding proteins. Over the past decade, this ubiquitously expressed protein has been extensively investigated in cancer research because it is involved in the regulation of mRNA stability and translation in many cell types. HuR activity and function is associated with its subcellular distribution, transcriptional regulation, translational and post-translational modifications. HuR regulation of target mRNAs is based on the interaction between the three specific domains of HuR protein and one or several U- or AU-rich elements (AREs) in the untranslated region of target mRNAs. A number of cancer-related transcripts containing AREs, including mRNAs for proto-oncogenes, cytokines, growth factors, and invasion factors, have been characterized as HuR targets. It has been proposed that HuR has a central tumorigenic activity by enabling multiple cancer phenotypes. In this review, we comprehensively survey the existing evidence with regard to the diverse functions of HuR in caner development and progression. The current data also suggest that HuR might be a novel and promising therapeutic target and a marker for treatment response and prognostic evaluation.
Highlights
HuR is a member of the embryonic lethal abnormal vision (ELAV) family of RNA-binding proteins (RBPs) originally identified in Drosophila as essential for neural development [1]
Increasing evidence supports HuR is the first RBP that is shown to play a critical role in carcinogenesis and cancer progression by functioning as either an oncogene or a tumor suppressor regulating the expression of various target genes
A comprehensive investigation of the biological activity of HuR indicates it is a crucial regulator of post-transcriptional gene expression and has a central role in cancer [171]
Summary
HuR is a member of the embryonic lethal abnormal vision (ELAV) family of RNA-binding proteins (RBPs) originally identified in Drosophila as essential for neural development [1]. It is the product of the human ELAVL1 gene located on human chromosome 19p13.2 and was first cloned in 1996 [2,3]. Increasing evidence supports HuR is the first RBP that is shown to play a critical role in carcinogenesis and cancer progression by functioning as either an oncogene or a tumor suppressor regulating the expression of various target genes. This review summarizes the recent findings and associations between HuR and cancer, especially in cancer development, progression, treatment responses, and prognosis
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