American Association for Cancer Research
Browse

Figure 5 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma

Download (826.04 kB)
figure
posted on 2025-02-19, 08:40 authored by Luiza Doro Pereira, Monica Wielgos-Bonvallet, Selim Misirlioglu, Alireza Khodadai-Jamayran, Petar Jelinic, Douglas A. Levine

PARPi–induced CXCL10 gene expression levels are not affected by STING knockdown in a cGAS-defective cell line. A, The expression levels of STING and cGAS were measured by western blot analysis 48 hours after DMSO treatment. ERK2 was used as a loading control. Results shown are from one of two independent experiments. B–E, OVCAR3 and CAOV3 were transfected with control or STING siRNA for 24 hours. Cells were re-plated the next day and treated 48 hours after transfection with DMSO, 10 μmol/L veliparib, or 2 μmol/L talazoparib. Total RNA was extracted from cell pellets that were collected 48 hours after drug treatment, and then 1 μg of RNA was reverse transcribed to cDNA. Quantitative real-time RT-PCR was utilized to measure the gene expression levels of TMEM-173 (STING), CXCL10, and GAPDH. T tests were performed between the control siRNA DMSO-treated group and the five other conditions. A t test was also performed between the control siRNA veliparib- vs. STING siRNA veliparib-treated groups and the control siRNA talazoparib- vs. STING siRNA talazoparib-treated groups. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; ns, not statistically significant.

History

ARTICLE ABSTRACT

This work highlights how different PARPis, especially talazoparib, modulate immune-related gene expression in ovarian cancer cells, independent of the cGAS-STING pathway. These findings may improve our understanding of how different PARPis affect the immune system in various genetic backgrounds.

Usage metrics

    Cancer Research Communications

    Licence

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC