CNPY2 is significantly overexpressed in liver cancer (HCC) and its levels are linked to poor survival outcomes in patients.
The deletion of Cnpy2 in mice prevents HCC development induced by a chemical carcinogen, showing its crucial role in liver cancer progression.
CNPY2 contributes to p53 destabilization and promotes oncogene expression through its interaction with ribosome proteins and enhancement of UPR pathways, indicating it as a potential therapeutic target for HCC.