Fig. 6: circSLC38A1 increased ILF3 expression via inhibition of protein degradation. | Cell Death & Disease

Fig. 6: circSLC38A1 increased ILF3 expression via inhibition of protein degradation.

From: Characterization of circSCL38A1 as a novel oncogene in bladder cancer via targeting ILF3/TGF-β2 signaling axis

Fig. 6

A Expression levels of ILF3 in BC cells with circSLC38A1 deficient or circSLC38A1 overexpression. B Protein level of ILF3 in UM-UC-3 cells over-expressed circSLC38A1, followed by 100 µg/ml CHX treatment for the indicated time points. C Protein level of ILF3 in circSLC38A1 knockdown T24 cells, followed by 100 µg/ml CHX treatment for the indicated time points. D, E Immunoblot analysis of ILF3 in polyubiquitination assays of 293 T cells transfected with the indicated constructs and treated with 20 µM MG132 for 6 h. Data represent mean ± SD from three independent experiments; *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

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