CD155 regulates the AKT/mTOR pathway, autophagy, and the NF-κB (NF-κB) pathway. (A) Phosphoproteome array analysis of phosphoprotein expression changes after CD155 knockdown in CaSki cells. Phosphoproteins whose levels increased or decreased by more than 12% are marked in red and blue, respectively. (B) Immunofluorescence staining of LC3B in CaSki and HeLa cells transfected with CD155 siRNA (si-CD155), negative control RNA (NC-CD155), or PCMV-CD155, Scale bar: 10 µm. (C) Western blot analysis of the protein levels of AKT, p-AKT, mTOR, p-mTOR, p-4EBP1, p-p70S6K, Beclin1, LC3I, LC3II, p-NF-κBp65, p-IKKα/β, and p-IKKγ in CaSki and HeLa cells transfected with NC-CD155, si-CD155, PCMV-NC, or PCMV-CD155. β-actin was used as a loading control. (D) The Co-IP results showed that CD155 interacted with AKT to form the CD155/AKT complex. The Co-IP and western blot results showed that in PCMV-CD155 CaSki and PCMV-CD155 HeLa cells, the abundance of the CD155/AKT complex was significantly increased. (E) Immunofluorescence for p-NF-κBp65, p-IKBα using CaSki and HeLa cells infected with CD155 siRNA (si-CD155), negative control RNA (NC-CD155), or PCMV-CD155, Scale bar: 10 µm. Data are the mean ± SEM of at least three independent experiments.