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Fig. 1 | Molecular Cancer

Fig. 1

From: PARP inhibitor Olaparib overcomes Sorafenib resistance through reshaping the pluripotent transcriptome in hepatocellular carcinoma

Fig. 1

PARP1 is activated in embryonic stem cells and the residual tumors after Sorafenib treatment and significantly potentiated Sorafenib both in vitro and in vivo. a The relative expression of PARP1 normalized to 3 endogenous control (combination of GAPDH, ACTB, and RPL13A) at different developmental stages including embryonic stem cell (ES), endoderm (EN), liver progenitor cell (LP), and premature hepatocytes (PH) was shown in boxplot. One-way ANOVA test. P < 0.0001. b Representative immunohistochemical staining of PARP1 in clinical HCC tumor tissues and their adjacent liver tissues. Distant liver (liver tissues > 1 cm from the tumor margin); Para-tumor, (liver tissues < 1 cm from the tumor margin), Scale bar, 100 μm. c IHC staining of PARP1 was performed in a tissue microarray (TMA) containing 196 liver tumor tissues from HCC patients. Kaplan-Meier analysis indicated that the staining score of PARP1 was significantly correlated with poor overall survival (P = 0.0068) (d) and disease-free survival (P = 0.0368) of HCC patients. e PLC-8024 cells (2 × 106 cells/mouse) were injected into nude mice at the right dorsal subcutaneously. The mice were randomly divided into four groups with different setup: treatment with PBS; Olaparib (50 mg/kg, thrice per week); Sorafenib (60 mg/kg, thrice per week) or both (n = 3). Tumor volumes were measured every three days. Data were shown as mean ± SD. f The apoptotic signals were detected by TUNEL staining of the tumor sections. Significant elevation of apoptosis was observed in tumors treated with both Sorafenib and Olaparib. g Tumor organoids derived from primary HCC patients (HCC-HK P1, HCC-HK P2) were treated with Olaparib (20 μM), Sorafenib (4 μM), or both, and their sensitivities to drug treatment were examined. *, P < 0.05, ***, P < 0.001, ****, P < 0.0001, independent t test

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