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USP8 activates HYCC1. 4 / 4
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"Consistent with the results identified above, USP8 WT promoted the proliferation, invasion, and stemness of HCC cells, but the C786A and S716A mutants lost these abilities (Figure 6H–L; Figure S7A–D, Supporting Information)."
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"In addition, USP8 depletion inhibited the proliferation, invasion and stemness of HCC cells and conferred ferroptosis resistance, which effects could be further rescued by beta-catenin overexpression."
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"Collectively, this study demonstrates that pharmacological inhibition or knockout of USP8 can inhibit the progression of HCC and induce ferroptosis via decreasing the stability of OGT, which imposes a great challenge that targeting of USP8 is a potential approach for HCC treatment."
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"Consistent with our previous observations of DUB‐IN‐3, knockout of USP8 significantly suppressed the proliferation, invasion, and stemness of HCC cells (Figure S1, Supporting Information)."
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