Dysregulation of TTP and HuR plays an important role in cancers.

Defects in the adenosine-uridine (AU)-rich elements (AREs), which mediate post-transcriptional regulation, play important roles in cancers. Both tristetraprolin (TTP, also known as TIS11 and ZFP36) and human antigen R (HuR, also known as ELAVL1) are two important and closely related AU-rich RNA-binding proteins (ARE-BPs). High-expression or aberrant nuclear/cytoplasmic distribution of HuR and decreased TTP have been found in many types of cancers. TTP mediates the decay of target mRNAs, whereas HuR generally stabilizes target transcripts and promotes translation of certain mRNAs. Furthermore, thousands of overlapping binding sites of TTP and HuR were found in more than 1300 genes. RNA-IP experiments also indicated that TTP can bind directly to and destabilize HuR mRNA. The dysregulation of TTP and HuR has been found to play an important role in the progression of cancers, including inflammation-related cancer, as well as in proliferation, apoptosis, angiogenesis, metastasis, invasion, and chemotherapy resistance. In this review, we provided an overview of the role of TTP and HuR, as well as the underlying mechanisms of the TTP-HuR axis in cancers.