Reprimo, TP53-dependent G2 arrest mediator homolog (RPRM)

Reprimo, TP53-dependent G2 arrest mediator homolog (RPRM), is a highly glycosylated cytoplasmic protein and secreted factor that acts primarily as a tumor suppressor downstream of the p53 pathway[1][2][4]. Originally identified as a p53-transcriptional target mediating cell cycle arrest at the G2/M checkpoint—via inhibition of Cdc2/cyclin B1 complex nuclear translocation—it restricts cell proliferation and survival and enhances apoptosis, especially under cellular stress[2][4]. RPRM is frequently epigenetically silenced (by promoter hypermethylation) in various cancers, linking its loss to uncontrolled cell growth and tumorigenesis[3][4]. Recent findings indicate RPRM is secreted and induces extrinsic apoptosis in neighboring cells through binding to specific protocadherin family receptors (FAT1, FAT4, CELSR1/2/3), activating the Hippo–YAP/TAZ–p73 proapoptotic pathway, a mechanism distinct from classical death ligand signaling[1]. Its methylation status serves as a promising biomarker for cancer diagnosis and monitoring of demethylating therapy effectiveness[3][4]. There are no widely reported interacting small-molecule drugs other than epigenetic modifiers. RPRM's essential biological roles, molecular targeting potential, and secreted nature suggest ongoing interest in its application for therapeutic development and cancer biomarker utility[1][2][3][4].

Other names

Protein reprimoFLJ90327REPRIMOcandidate mediator of the p53-dependent G2 arrestTP53-dependent G2 arrest mediator candidate

Restoration of tumor suppression by reversing epigenetic silencing (demethylating drug-induced); Induction of extrinsic apoptosis in recipient cells through activation of the Hippo–YAP/TAZ–p73 axis via interaction with protocadherin family receptors (FAT1, FAT4, CELSR1, CELSR2, CELSR3)