The stabilization of HuR not only activates the STAT3/Wnt signaling pathway to promote CRC cell survival and proliferation and suggests a potential link between CRC and chronic inflammation through lncRNAs R. Furthermore, lncRNA SPRY4-IT1 can enhance HuR’s interaction with mRNA related to tight junction (TJ) proteins, promoting the expression of claudin-1, claudin-3, occludin, and JAM-1, thus maintaining intestinal epithelial barrier function and inhibiting tumorigenesis and progression (94). This evidence concerns the gene STAT3 and colorectal carcinoma.