IndraLab

Statements

P5091 inhibits CCDC6. 10 / 10
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"In a recent study, P5091, an inhibitor of USP7, promoted CCDC6 degradation and sensitized bladder cancer cells to the cytotoxic effect of the PARP-inhibitor olaparib (128)."
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"In order to evaluate whether the new epigenetic agent RRx-001, that induce DNA damage through the release of reactive oxygen or nitrogen species, combined with P5091, that downregulates CCDC6 and impairs HR-DNA repair, might increase the sensitivity to PARPi in urothelial carcinoma cells, we treated the bladder cancer cells with different concentrations of the PARP-inhibitor Olaparib and with fixed doses of P5091 and RRx-001."
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"Generally, CCDC6 downregulation by P5091 improved sensitivity to olaparib in all cell lines herein analysed."
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"Notably, the CCDC6 downregulation by P5091 treatment affected PARGi-induced cytotoxicity (in the presence of P5091 at 2.5 μM, the IC50 raised to 1.33 μM ± 0.32) (Fig. 3A)."
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"The P5091 accelerated the degradation of CCDC6 in PC3 cells and LNCaP versus control cycloheximide alone treated."
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"Interestingly, in the presence of P5091, which increases the CCDC6 degradation, the combined treatment of cisplatin and olaparib turned into an additive effect in OV-90olaR cells (CI = 1) (Fig. 4E)."
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"Upon the CCDC6 degradation induced by P5091, the cells sensitivity to PARP-inhibitor was evaluated by cell viability assays."
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"Moreover, P5091 accelerated the degradation of CCDC6 sensitizing the cells to PARP-inhibitors, that acted sinergistically with genotoxic agents."
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"Moreover, in high-grade urothelial bladder cancer, the CCDC6 degradation caused by P5091 making bladder cancer cells more sensitive to PARP-inhibitor drugs [86]."
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"Thus, P5091 accelerated the degradation of CCDC6 versus control cycloheximide alone treated H526 and H209 L-NET cells."
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