Fig. 4: TRIM52 expression promoted the activation of NF-kB signal pathway in ovarian cancer.

a The mRNA level of NF-kB P65 in 40 pairs of ovarian cancer and normal tissue was detected by qPCR. Positive log₂ (tumor/normal) on the y-axis indicated increasing expression of NF-kB P65 in a tumor tissue. b Pearson’s correlation analysis of TRIM52 and NF-kB P65 in 40 ovarian cancer specimens. Proteins levels of IKKβ and IKBα and phosphorylated IKKβ and IKBα were evaluated by western blot in treated SKOV3/CAOV3 cells with TRIM52-Ri2,3 (c, d) and in infected HO8910 cells by synthetic TRIM52 lentivirus (e). Nuclear protein P65 expressions were detected by WB similarly in treated SKOV3/ CAOV3 cells (f, g) and in infected HO8910 cells (h). Protein levels of NF-kB downstream effectors including MMP9, Bcl2, caspase 3, IL8, and TNFα were detected by WB in SKOV3/CAOV3 cells with TRIM52 knockdown (i, j) and in HO8910 cells infected with TRIM52 lentivirus (k). mRNA expressions of MMP9, Bcl2, caspase 3, IL8, and TNFα were confirmed by qPCR in treated SKOV3/CAOV3 cells with TRIM52-Ri2,3 (l, m) and in HO8910 cells infected with TRIM52 lentivirus (n). Nuclear protein P65 and plasmosin P65 protein expressions were evaluated by WB in SKOV3 cells treated by TRIM52-Ri3 plus LPS (an activator of NF-kB P65) (o) and in HO8910 cells treated by TRIM52 lentivirus plus PDTC (an inhibitor of NF-kB P65) (p). Proteins expressions of MMP9, Bcl2, caspase 3, IL8, and TNFα were confirmed by WB in TRIM52-knockdown SKOV3 cells with LPS (q) and overexpressing-TRIM52 HO8910 cells with PDTC (r). *P < 0.05, **P < 0.01, ***P < 0.001, versus NC or vector