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Transcriptome-wide induction of inflammatory response after radiation and PARP7 inhibition in PDAC cells (A, B) Quantification of differentially expressed (A) genes or (B) repetitive elements (fold-change>2, p < 0.05) in BxPC-3 and PANC-1 cells treated with 3 × 8 Gy without or with the PARP7 inhibitors KMR-206 (300 nM) and RBN-2397 (1 μM). PARP7 inhibitors were added 24 h before irradiation and kept until harvesting 72 h after the last irradiation. (A) Upregulated genes are shown in red, downregulated genes in blue. (B) Different categories of repetitive elements are shown with different colors. (C) Log2 fold changes in gene expression between indicated treated and control samples of most strongly upregulated repetitive elements. (D) Normalized enrichment scores (NESs) from gene set enrichment analysis (GSEA) for Hallmark gene sets (MSigDB) between indicated treatments and controls in PDAC cells. Shown are pathways significant in at least 3 comparisons with significance level p < 0.05 adjusted for multiple testing. (E) Log2 fold changes in gene expression between indicated treated and control samples of chosen genes involved in immune signaling or cell death pathways. The experiments were performed in three biological replicates.
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Image Search Results


Transcriptome-wide induction of inflammatory response after radiation and PARP7 inhibition in PDAC cells (A, B) Quantification of differentially expressed (A) genes or (B) repetitive elements (fold-change>2, p < 0.05) in BxPC-3 and PANC-1 cells treated with 3 × 8 Gy without or with the PARP7 inhibitors KMR-206 (300 nM) and RBN-2397 (1 μM). PARP7 inhibitors were added 24 h before irradiation and kept until harvesting 72 h after the last irradiation. (A) Upregulated genes are shown in red, downregulated genes in blue. (B) Different categories of repetitive elements are shown with different colors. (C) Log2 fold changes in gene expression between indicated treated and control samples of most strongly upregulated repetitive elements. (D) Normalized enrichment scores (NESs) from gene set enrichment analysis (GSEA) for Hallmark gene sets (MSigDB) between indicated treatments and controls in PDAC cells. Shown are pathways significant in at least 3 comparisons with significance level p < 0.05 adjusted for multiple testing. (E) Log2 fold changes in gene expression between indicated treated and control samples of chosen genes involved in immune signaling or cell death pathways. The experiments were performed in three biological replicates.

Journal: Molecular Therapy Oncology

Article Title: PARP7 inhibitors enhance the immunogenic effects of radiation in pancreatic cancer cells

doi: 10.1016/j.omton.2026.201258

Figure Lengend Snippet: Transcriptome-wide induction of inflammatory response after radiation and PARP7 inhibition in PDAC cells (A, B) Quantification of differentially expressed (A) genes or (B) repetitive elements (fold-change>2, p < 0.05) in BxPC-3 and PANC-1 cells treated with 3 × 8 Gy without or with the PARP7 inhibitors KMR-206 (300 nM) and RBN-2397 (1 μM). PARP7 inhibitors were added 24 h before irradiation and kept until harvesting 72 h after the last irradiation. (A) Upregulated genes are shown in red, downregulated genes in blue. (B) Different categories of repetitive elements are shown with different colors. (C) Log2 fold changes in gene expression between indicated treated and control samples of most strongly upregulated repetitive elements. (D) Normalized enrichment scores (NESs) from gene set enrichment analysis (GSEA) for Hallmark gene sets (MSigDB) between indicated treatments and controls in PDAC cells. Shown are pathways significant in at least 3 comparisons with significance level p < 0.05 adjusted for multiple testing. (E) Log2 fold changes in gene expression between indicated treated and control samples of chosen genes involved in immune signaling or cell death pathways. The experiments were performed in three biological replicates.

Article Snippet: Apoptosis, necroptosis, and ferroptosis were inhibited using Q-VD-Oph (10 μM; TargetMol Chemicals), necrostatin-1 (10 μM; TargetMol Chemicals) and liproxstatin-1 (5 μM; TargetMol Chemicals), respectively.

Techniques: Inhibition, Irradiation, Gene Expression, Control, Analysis, RNA Sequencing