Fig. 4
cGAS-STING signaling pathway is involved in the PARP inhibitor-induced cellular senescence in HRP cancer cells. (A) (B) Gene expression of of IL1B, IL6, and CXCL10 in the PARP inhibitor-treated cells. HeLa cells (A) and A-549-reproter cells (B) were treated with olaparib at the indicated concentrations for 72 h. qRT-PCR for IL1B, IL6, and CXCL10 was performed. (C) IL1B gene expression in olaparib-treated HRP cells. A549, OVISE, SKOV3, and MCAS cells were treated with olaparib at the indicated concentrations for 72 h. qRT-PCR for IL1B was performed. (D) IFNB1 and TNFSF15 gene expressions in olaparib-treated HRP OC cells. OVISE, SKOV3, and MCAS cells were treated with olaparib at 10 μM for 72 h. qRT-PCR for NFB1 and TNFSF15 was performed. (E) Immunofluorescence of cGAS in olaparib-treated cells. A549 and SKOV3 cells were treated with olaparib at 10 μ M for 72 h. Red, green, and blue signals indicate cGAS, Lamin B1, and DAPI, respectively. White arrows indicate the localization of cGAS in micronuclei. Scale bars indicate 50 μm. (F) IRF-Luc activity in STING-knockout (KO) cells in treatment with olaparib. The STING KO (gray bars) and negative KO (black bars) A549-reporter cells were treated with DMSO and olaparib at 10 μM for 72 h, followed by IRF reporter assay. Data are shown as means ± SD (n = 3).
