Research Paper Advance Articles

Inhibiting USP8 overcomes hepatocellular carcinoma resistance via suppressing receptor tyrosine kinases

The inhibitory effects of genetic knockdown of USP8 in HCC. (A) USP8 protein level in USP8-depleted HCC cells. USP8 knockdown inhibits proliferation (B) and induces apoptosis (C) in HuH6 and HepG2 cells, and significantly enhances the efficacy of doxorubicin (Dox) and sorafenib (Sor). (D) USP8 protein level in USP8-depleted doxorubicin-resistant HCC cells. USP8 knockdown inhibits proliferation (E) and induces apoptosis (F) in HuH6-r and HepG2-r cells. Doxorubicin at 0.1 μM and sorafenib at 0.5 μM were used. Cells were harvested for USP8 protein level analysis at 48 hours post-transfection. Drugs were added to cells at 48 hours post-transfection. Cell proliferation and apoptosis were determined after 3 days treatment. *p

Figure 2. The inhibitory effects of genetic knockdown of USP8 in HCC. (A) USP8 protein level in USP8-depleted HCC cells. USP8 knockdown inhibits proliferation (B) and induces apoptosis (C) in HuH6 and HepG2 cells, and significantly enhances the efficacy of doxorubicin (Dox) and sorafenib (Sor). (D) USP8 protein level in USP8-depleted doxorubicin-resistant HCC cells. USP8 knockdown inhibits proliferation (E) and induces apoptosis (F) in HuH6-r and HepG2-r cells. Doxorubicin at 0.1 μM and sorafenib at 0.5 μM were used. Cells were harvested for USP8 protein level analysis at 48 hours post-transfection. Drugs were added to cells at 48 hours post-transfection. Cell proliferation and apoptosis were determined after 3 days treatment. *p<0.01, compared to control. #p<0.01, compared to doxorubicin or sorafenib alone.