Hnrnpab, also known as heterogeneous nuclear ribonucleoprotein A/B, is an RNA-binding protein closely associated with RNA biological function and metabolism [4]. It is involved in various cellular processes such as RNA splicing, nuclear export, and sensing of RNA [5].

In pancreatic ductal adenocarcinoma (PDAC), hnRNPAB is highly expressed, promoting cell migration, invasion, and liver metastasis. Deprivation of hnRNPAB in xenograft tumor mouse models significantly attenuated liver metastasis. It binds to MYC mRNA, prolonging its half-life and promoting PDAC cells to secrete CXCL8 via MYC, which facilitates tumor cells entering the hepatic parenchyma [1].

In non-small cell lung cancer (NSCLC), knockdown of hnRNPAB in stable cell lines inhibited cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), arresting the cell cycle at G1 phase [4].

In colorectal cancer stem cells, knockdown of hnRNPAB reduced stem cell properties and enhanced chemosensitivity [6].

In influenza A virus infection, hnRNPAB-deficient mice display higher viral burdens, enhanced cytokine production, and increased mortality. HnRNPAB interacts with NP of IAV to inhibit the interaction between PB1 and NP, disturbing polymerase activity and inhibiting virus replication [2].

In the development of the central nervous system, Hnrnpab-/-mouse brains show impaired neural cell migration from the subventricular zone (SVZ), and Eps8, a gene related to cell motility, is decreased in Hnrnpab-/-SVZ tissue [3].

In conclusion, Hnrnpab plays crucial roles in multiple biological processes and disease conditions. Gene-knockout models, especially in mice, have revealed its functions in cancer metastasis, cell proliferation, virus infection, and neural cell migration. Understanding Hnrnpab can potentially provide new therapeutic targets for cancers like PDAC, NSCLC, and colorectal cancer, as well as insights into anti-influenza defense mechanisms.