ELAV-like protein 1 (HuR) (HuR)

ELAV-like protein 1 (HuR) is a ubiquitously expressed RNA-binding protein that serves as a master regulator of post-transcriptional gene expression by binding to AU-rich elements (AREs) in the 3' untranslated regions of target mRNAs [1]. This interaction stabilizes the mRNA transcripts, protecting them from rapid degradation and facilitating their translation into proteins that drive cell proliferation, survival, and inflammation [2]. In healthy cells, HuR is primarily nuclear, but in many pathological states, particularly cancer, it translocates to the cytoplasm where it exerts its stabilizing effects on oncogenic mRNAs such as those encoding VEGF, COX-2, and various cyclins [3]. High levels of cytoplasmic HuR are frequently associated with poor prognosis and resistance to therapy in a wide range of malignancies [4]. Therapeutic strategies targeting the HuR-mediated mRNA stabilization machinery involve small molecules, such as MS-444 and CMLD-2, which disrupt HuR-RNA binding or inhibit HuR dimerization and translocation [5]. While targeting HuR offers a potent way to simultaneously downregulate multiple pro-survival pathways, the broad regulatory role of HuR in normal physiology presents challenges regarding potential systemic toxicity and off-target effects [6].

Other names

ELAVL1Human antigen RHu-antigen RMelGELAV-like RNA-binding protein 1

Inhibition of HuR-mRNA binding by competing for the RNA-binding domain, or inhibition of HuR homodimerization and nucleocytoplasmic translocation [5].