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Fig. 5 | Cancer Cell International

Fig. 5

From: FBXL18 promotes endometrial carcinoma progression via destabilizing DUSP16 and thus activating JNK signaling pathway

Fig. 5

FBXL18 targeted DUSP16 as a ubiquitination substrate. (A-B) The results of Co-IP and western blotting assays revealed the endogenous and exogenous interaction of FBXL18 and DUSP16. (C-D) qRT-PCR analysis of DUSP16 mRNA levels after silencing or overexpressing FBXL18 in KLE and Ishikawa cells. (E-F) Western blot analysis of DUSP16 protein level in EC cells of shNC and shFBXL18 groups, and quantitative analysis. (G-H) Western blot analysis of DUSP16 protein level in EC cells after overexpressing FBXL18, and quantitative analysis. (I-J) DUSP16 protein half-life in EC cells of LV-Control and LV-FBXL18 groups were evaluated by CHX chase assay. (K-L) Comparison of DUSP16 protein half-life in EC cells stably knockdown of FBXL18 and control cells. (M-N) The ubiquitination status of endogenous DUSP16 after silencing or overexpressing FBXL18 in EC cells were determined by immunoprecipitation and western blotting. *P < 0.05; **P < 0.01; ***P < 0.001

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Cancer Cell International

ISSN: 1475-2867

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