B-cell translocation gene 3 (BTG3)

B-cell translocation gene 3 (BTG3) is a member of the BTG/Transducer of ErbB2 (Tob) family of antiproliferative proteins that acts as a tumor suppressor through multiple mechanisms. BTG3 is a transcriptional regulator induced by p53 and is involved in maintaining genomic stability via regulation of checkpoint kinase 1 (CHK1) activation and chromatin association, and by inhibiting E2F1 transcriptional activity to block cell cycle progression. BTG3 interacts with AKT and other signaling molecules to inhibit proliferation, migration, invasion, angiogenesis, and promote apoptosis, thus limiting neoplastic progression and metastasis. Down-regulation or loss of BTG3 expression has been observed in a spectrum of human cancers and correlates with poor prognosis, advanced disease stage, and metastasis. BTG3 encoded protein is primarily nuclear and exerts its effects by protein-protein interactions via its N-terminal conserved domains (Box A and B) and a divergent C-terminus conferring unique functions; for example, controlling DNA repair via XPC mobility and nuclear translocation of VCP/p97. Currently, BTG3 is not directly targeted by any approved drugs, but its expression status may serve as a biomarker for prognosis and therapeutic stratification in oncology.

Other names

ANATOB5tob55APRO4ANA/BTG3abundant in neuroepithelium area proteinBTG family member 3protein Tob5TOFAprotein BTG3

Not established for drugs; BTG3 itself regulates checkpoint kinase 1 (CHK1) activation, AKT signaling, E2F1 transcription factor activity, genomic stability, and cellular senescence, thus suppressing proliferation and tumorigenesis.