A-kinase-interacting protein 1 overexpression correlates with deteriorative tumor features and worse survival profiles and promotes cell proliferation but represses apoptosis in NSCLC.
Treatment with a CBP inhibitor ICG-001 effectively inhibited the metastatic progression of HCC tumors that had elevated AKIP1 in both cell line and patient-derived xenograft mouse models.
DFS was worse in patients with tumor tissue AKIP1 high expression compared with patients who had AKIP1 low expression in total patients (P < .001), TNM stage I (P < .001) and TNM stage III (P < .001) patients.
In summary, these findings suggested that BCA3 is a novel protein partner of TAp73, and they cooperate with each other to exert tumor-suppressive functions and sensitize the response of cervical cancer cells to radiotherapy.