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. 2019 Jan 27;15(7):1130–1149. doi: 10.1080/15548627.2019.1570063

Figure 9.

Figure 9.

Deubiquitination and phosphorylation of UVRAG promotes HCC cell proliferation and tumorigenesis by decreasing EGFR degradation. UVRAGS522A mutation (b) enhances while UVRAGK517,559R (a) delays EGFR degradation. Huh7 cells stably transduced with empty vector or UVRAG constructs were starved of serum 24 h and then added with EGF (200 ng /ml) for the indicated time. EGFR level in cell lysate was measured by immunoblotting. The band intensity was measured and shown. (c) UVRAGS522A mutation inhibits whereas UVRAGK517,559R promotes Huh7 cell proliferation. Huh7 cells stably expressing vector control and UVRAG constructs were seeded at the same number per well. Then CCK-8 assay was performed every 24 h. (d) UVRAGS522A mutation significantly inhibits while UVRAGK517,559R promotes colony formation of Huh7 cells. Huh7 cells stably expressing vector control and UVRAG constructs were used for colony formation assays. UVRAGS522A mutation (e) significantly inhibits while UVRAGK517,559R (g) promotes tumor growth in mice. (n = 10/group). The effect of UVRAG-S522A mutation (f) and UVRAGK517,559R (h) on tumor weight relative to the whole body weight was analyzed.