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. 2021 Feb 8;8(8):2002874. doi: 10.1002/advs.202002874

Figure 7.

Figure 7

OTUD1 deubiquitinates and stabilizes DCAF10. A,B) Relative protein expression levels of DCAF10 in a pulse‐chase assay performed in the indicated A) KYSE30 or B) KYSE150 cells. Quantification of DCAF10 expression relative to β‐actin expression is shown. The data are the means ± s.e.m.; n  =  3. C,D) IB to assess MCL1 ubiquitination in the indicated C) KYSE150 or D) KYSE30 cells (D1:OTUD1; shDC: shDCAF10; shCU: shCUL4A; shDD: shDDB1). E) IB for OTUD1, DCAF10, MCL1, and AIF expression in ESCC cell lines. F) IB to assess Myc‐DCAF10 ubiquitination in 293T cells cotransfected with Myc‐DCAF10, HA‐Ub mutants and V5‐OTUD1. K48 and K63 indicate that all lysines except K48 or K63 were mutated to arginines. G) Tumor weights of xenografts from the indicated cells (KYSE150 background). The data are the means ± s.e.m.; n  =  7. Two‐tailed t tests, ***p < 0.001, ns: not significant. H) Tumor weights of xenografts from the indicated cells (KYSE150 background) and treated with DDP, Z‐VAD, or S63845. The data are the means ± s.e.m.; n  =  7. Two‐tailed t tests, ***p < 0.001, **p < 0.01, ns: not significant. I) A schematic model showing the overlapping and distinct downstream events of OTUD1 overexpression and loss. OTUD1 overexpression not only activates both parthanatos and caspase‐dependent apoptosis pathways, but also compromises OXPHOS to further promotes cell death. In contrast, OTUD1 loss inhibits DDP‐induced apoptosis by suppression of parthanatos and caspase‐dependent apoptotic pathway.