Fig. 5: TRIM11 promoted the protein level of β-catenin to directly upregulate ABCC9. | Oncogenesis

Fig. 5: TRIM11 promoted the protein level of β-catenin to directly upregulate ABCC9.

From: TRIM11 facilitates chemoresistance in nasopharyngeal carcinoma by activating the β-catenin/ABCC9 axis via p62-selective autophagic degradation of Daple

Fig. 5

a Overexpression of TRIM11 significantly increased TOPflash/FOPflash luciferase reporter activity in CNE2 cells, while KO of TRIM11 significantly suppressed Wnt activity in CNE2-DDP cells. **P < 0.01. b Western blot analysis results showed that TRIM11 expression enhanced the expression of ABCC9 and β-catenin, while KO of TRIM11 showed the opposite effect. c The mRNA levels of β-catenin were detected after overexpressing TRIM11 in CNE1 and CNE2 cells. d, e The protein level of β-catenin increased in the cytoplasm and nucleus, as demonstrated by confocal immunofluorescence analysis in CNE1 and CNE2 cells after stably overexpressing TRIM11. Scale bar, 20 µm. f The TCF/LEF motif is shown. g Schematic illustration of the WT TCF/LEF motif sequences within the ABCC9 promoter and its mutants for luciferase reporter assays. h CNE2 cells stably transfected with an empty vector or TRIM11-encoding plasmid were transfected with a luciferase reporter plasmid in which luciferase expression was driven by a WT or mutant ABCC9 promoter. Luciferase activity was measured as described in the “Materials and methods” section. Data are the mean ± SD of triplicate samples. **P < 0.01. i Cells were analyzed in ChIP assays using anti-β-catenin antibody as described in the “Materials and methods” section.

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