Fig. 7: USP10 inhibitor improves the efficacy of PARP1 inhibitor in breast cancer. | Oncogene

Fig. 7: USP10 inhibitor improves the efficacy of PARP1 inhibitor in breast cancer.

From: The deubiquitination-PARylation positive feedback loop of the USP10-PARP1 axis promotes DNA damage repair and affects therapeutic efficacy of PARP1 inhibitor

Fig. 7

A MCF7 cells were treated with or without Spautin-1 (20 μM) or Olaparib (10 μM) for 24 h. Cells were stained with 7-AAD and APC-Annexin V and analyzed by FACS, ***P < 0.001. B MCF7 cells were treated with or without Spautin-1 (20 μM) or Rucaparib (10 μM) for 24 h. Cells were stained with 7-AAD and APC-Annexin V and analyzed by FACS, ***P < 0.001. C MCF7 cells transfected with or without PARP2 siRNA for 48 h were treated with or without Spautin-1 (10 μM) and Olaparib (10 μM) for 24 h. Cells were stained with 7-AAD and APC-Annexin V and analyzed by FACS; N.S., not significant. D, E Cell viability of MCF7 cells treated with or without Spautin-1 (20 μM) and Olaparib or Rucaparib at the indicated concentrations for 24 h. Cell viability was assessed by CCK8 assay. F MCF7 cells treated with Spautin-1 (20 μM), with or without different dose of PARP1 inhibitor Olaparib for 24 h. The representative images of cell colonies were shown. G The survival outcome analysis of patients with breast cancer in response to Olaparib treatment according to The Cancer Genome Atlas (TCGA) data. Correlation of USP10 and PARP1 expression in human breast cancer (H), ovarian cancer (I), pancreatic cancer (J) and prostate cancer (K) in the GEPIA database. Tumor growth assay in nude mice subcutaneously inoculated with MCF7 cells. The mice were treated with or without Spautin-1 (10 mg/kg) and Olaparib (40 mg/kg). The images of tumors were acquired (L), and their volume (M) and weight (N) were determined. Data are shown as mean ± SD (n = 5 for each group). ***P < 0.001.

Back to article page