Abstract
Pinin is a moonlighting protein localized in desmosomes and nucleus. It could promote the growth of hepatocellular carcinoma. Whether this protein can induce epithelial-to-mesenchymal transition (EMT) and malignant progression in HCC is unknown. This work found that Pinin prompts EMT in vitro and in vivo. Further mechanism study found that Pinin increases the level of N6-methyladenosine (m6A) modification of RNA by interacting with METTL3, which in turn induces snail1 expression. These findings suggest that Pinin induces EMT by regulating m6A modification and, thus, could be a potential anticancer target for HCC therapy.