Previous studies reported that HuR was a downstream target of miR-29b in some cancer cells: miR-29b inhibits expression of HuR post-transcriptionally, thus playing a role in the regulation of intestinal epithelial cells (IECs) proliferation and intestinal epithelial homoeostasis [14]; miR-29 interacted directly with HuR, decreased miR-29 abundance correlated with increased activity of NF-κB in sarcoma cell lines [15]. This evidence concerns the gene NFKB1 and cancer.