The results also revealed increased levels of P65 and signal transducer and activator of transcription 3 (STAT3) phosphorylation and increased secretion of interleukin‑6 (IL‑6) and tumor necrosis factor‑α (TNF‑α) in CRC tissue compared with levels in precancerous tissue.
This study tries to investigate the effect of MTDH gene up-regulation on the activation of EMT in colorectal cancer (CRC) cells and identify the role of NF-κB p65.
COMMD10 targets p65 NF-κB (nuclear factor-κB) subunit and reduces its nuclear translocation, thereby leading to the inactivation of NF-κB pathway and suppression of CRC invasion and metastasis.
Blocking of NF-κB signaling by p65 siRNA interference was carried out to explore the mechanism of NDRG1 involving in epithelial-mesenchymal transition (EMT)-regulated invasion and metastasis of CRC.
We detected IGFBP-2 in a unique organization at the bottom of human colonic crypts in normal mucosa and at increased levels throughout human CRC tissue samples co-localizing with the phosphorylated p65 subunit of NF-κB.