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.
The DNA sequence for one of these breast cancer associated genes was used to construct the larger 1319 bp BCA3 cDNA sequence using ESTs without assigned names or functions.
A-kinase-interacting protein 1 overexpression correlates with deteriorative tumor features and worse survival profiles and promotes cell proliferation but represses apoptosis in NSCLC.
Knockdown of AKIP1 inhibited NSCLC cell migration, invasion and epithelial-mesenchymal transition (EMT), as indicated by the up-regulation of mesenchymal markers (fibronectin and vimentin) and down-regulation of epithelial marker E-cadherin, whereas overexpression of AKIP1 showed the opposite effects.
The DNA sequence for one of these breast cancer associated genes was used to construct the larger 1319 bp BCA3 cDNA sequence using ESTs without assigned names or functions.
Hence, these findings indicate an important role for AKIP1 in ESCC angiogenesis and lymphangiogenesis, and uncover a novel mechanism for the upregulation of VEGF-C in cancers.
We confirmed evidence for the importance of the Nkx2-8/AKIP1/NF-κB axis identified in ESCC cell models through an immunohistochemical analysis of a large cohort of human ESCC specimens.