Banf1 depletion inhibited proliferation and induced mitotic arrest in TNBC cells via loss of nuclear envelope integrity and aberrant nuclear morphology, inducing TNBC tumour cell-specific cell death. These findings highlight the significant overexpression and functional involvement of Banf1 in TNBC progression and suggests that it may have potential as a novel anti-cancer target, supporting further investigation.
The study offers insights into CRC's molecular mechanisms and proposes targeting the VRK1/BANF1/GLI1 axis as a potential therapeutic strategy. This method could result in more effective treatments for advanced CRC.
We showed that overexpression of PYCR1 and BANF1 and decreased expression of STARD8 in GC tissues was associated with poor prognosis and GC progression.
BANF1 is a key regulator of antitumor immunity mediated by cGAS-STING pathway. Therefore, our study provides a rational that targeting BANF1 is a potent strategy for enhancing immunotherapy for cancer with BANF1 upregulation.