Fig. 2: Suppressing USP8 in the ARID1A-deficient OCCC xenograft model exerts antitumor effects. | npj Precision Oncology

Fig. 2: Suppressing USP8 in the ARID1A-deficient OCCC xenograft model exerts antitumor effects.

From: Targeting USP8 causes synthetic lethality through degradation of FGFR2 in ARID1A-deficient ovarian clear cell carcinoma

Fig. 2

A, B Viability of ARID1A-proficient RMG-I-shNT and RMG-I-shUSP8 cells (A) and ARID1A-deficient OVISE-shNT and OVISE-shUSP8 (B) cells treated with 1 μg/mL Dox. Cells were treated with 1 μg/mL Dox for 48 h, and GFP-positive cells were detected (Day 0). Then, every 2–3 days, the cells were reseeded and treated with 1 μg/mL Dox, and GFP-positive cells were detected again. The percentage of GFP-positive cells relative to that on Day 0 was calculated to measure cell viability. Data are presented as the mean ± SEM (n = 3 independent samples). C, D Tumor volume (C) and tumor weight (D) of xenografts derived from ARID1A-deficient OVISE-shNT cells isolated from mice treated without or with Dox. Data are presented as the mean ± SEM: -Dox (n = 4 biologically independent mice per group), +Dox (n = 4 biologically independent mice per group). E, F Volume (E) and weight (F) of tumor xenografts derived from ARID1A-deficient OVISE-shUSP8 cells harvested from mice treated without or with Dox. Data are presented as the mean ± SEM: -Dox (n = 6 biologically independent mice per group), +Dox (n = 8 biologically independent mice per group).

Back to article page