Zfp36l1, a member of the RNA-binding zinc finger protein 36 (ZFP36) family, contains tandem CCCH-type zinc-finger motifs. It is an mRNA-binding protein that destabilizes mRNAs containing adenylate-uridylate-rich elements (AREs) in their 3'-untranslated regions (3'UTR), playing a crucial role in post-transcriptional regulation of gene expression and participating in numerous physiological processes [1,2,3,4,5,6,7,8,9,10].

In various disease models, Zfp36l1 shows diverse functions. In small cell lung cancer (SCLC), LSD1 represses Zfp36l1, and upon LSD1 inhibition, Zfp36l1 expression restores, blocking SCLC neuroendocrine differentiation by destabilizing SOX2 and INSM1 mRNAs [1]. In osteosarcoma, low Zfp36l1 expression promotes lung metastasis by inhibiting the SDC4-TGF-β signaling feedback loop [4]. In alcoholic liver disease, liver-specific Zfp36l1-deficient mice are protected from alcohol-induced hepatic steatosis, injury, and inflammation, possibly by stabilizing Fgf21 mRNA [5]. In chronic myeloid leukemia cells, Nuclease technology-derived knockout of Zfp36l1 leads to decreased proliferation rates, and Zfp36l1 negatively regulates the cell cycle inhibitor CDKN1A [9]. In flavivirus infection, overexpression of Zfp36l1 reduces Japanese encephalitis virus and dengue virus infection by destabilizing the viral genome via 5'-3' XRN1 and 3'-5' RNA-exosome RNA decay pathways [10].

In conclusion, Zfp36l1 is a key regulator in post-transcriptional gene regulation. Through gene knockout and other in vivo models, it has been shown to play important roles in multiple disease areas, including cancer, liver disease, and viral infection. These findings provide insights into the molecular mechanisms of these diseases and potential therapeutic targets.