Fig 1: ASPP1 represses Snail2 expression via inhibiting NF-?B pathway.Fold changes in NF-?B reporter activity in HCT116 (a) or HKe3 ER:HRAS V12 cells (b) with the indicated treatments. NF-?B reporter luciferase readings normalized to Renilla in control cells were used to set the baseline value at unity. Data are mean ± s.d. n = 3 samples per group. **P < 0.01. ***P < 0.001. c Total cell lysates from HCT116 cells were immunoprecipitated (IP) with an anti-p65 antibody or control IgG. ASPP1, p65, NF-?B1 p50 and NF-?B2 p52 levels are indicated. d HCT116 cells transfected with control or ASPP1 RNAi were immunoprecipitated with an anti-p65 antibody or control IgG. NF-?B1 p50, p65 and ASPP1 levels are indicated. ß-tubulin was used as a loading control. Scores under the bands are relative levels when compared with control cells (1.0). e Protein expression of E-cadherin, Snail2, p65 and ASPP1 in HCT116 cells with indicated treatment. ß-tubulin was used as a loading control. f Diagram showing ASPP1 represses EMT via inhibiting NF-?B-Snail2 pathway in CRC.