Fig. 6

TRIM22 and NOD2 interaction restricted EC progression by inhibiting the NF‑κB pathway. (A) NOD2 expression level in the normal endometrial tissue and EC tissues in TCGA database. (B) NOD2 expression level in EC tissues from the different stage (I, II, III, IV). (C) The Kaplan-Meier analysis between NOD2 and survival of EC patients in TCGA database. (D) Immunofluorescent detection of TRIM22 and NOD2 in EC and normal endometrial tissue. Scale bar, 20 μm. (E) Statistical analysis of TRIM22 in (D). (F)Statistical analysis of NOD2 in (D). (G) Co-IP detection of TRIM22, NOD2 and HA-Ub in TRIM22 OE and scramble control Ishikawa cells. (H) Reciprocal Co-IP detection of TRIM22, NOD2 and HA-Ub in TRIM22 OE and scramble control Ishikawa cells. (I) Immunoblots of TRIM22, NOD2, NF‑κB-p65, IκB-α, p-NF‑κB-p65, p-IκB-α in TRIM22 OE and scramble control Ishikawa cells. (J) Immunoblots of nuclear NF‑κB-p65 and cytoplasmic NF‑κB-p65 in TRIM22 OE and scramble control Ishikawa cells. (K) Representative images showing Edu incorporation in the scramble control and NOD2 KD Ishikawa cells. (L) Ratio of Edu-positive scramble control and NOD2 KD Ishikawa cells in (K). (M) Representative images of scramble control and NOD2 KD Ishikawa cells that cultured in trans-well plates. (N)The average number of migration Ishikawa cells in (M). (O) The average number of invasion Ishikawa cells in (M). (P) Representative images showing Edu incorporation in the scramble control, NOD2 KD and NOD2 KD + TRIM22 OE Ishikawa cells. (Q) Ratio of Edu-positive scramble control, NOD2 KD and NOD2 KD + TRIM22 OE Ishikawa cells. (R) Representative images of scramble control, NOD2 KD and NOD2 KD + TRIM22 OE Ishikawa cells. that cultured in trans-well plates. (S) The average number of migration Ishikawa cells in (R). (T) The average number of invasion Ishikawa cells in (R). Data were expressed as means ± SEM of three independent experiments. Scale bar, 50 μm. *p < 0.05, **p < 0.01, ***p < 0.001