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Quantitative RNAseq Analysis of Treatment Outcomes with Talazoparib, Romidepsin or Combination in MBL2 cell line

ABSTRACT: Quantitative RNAseq Analysis of Treatment Outcomes with Talazoparib, Romidepsin or Combination in MBL2 cell line

PROVIDER: PRJNA661301 | ENA |

REPOSITORIES: ENA

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Quantitative RNAseq Analysis of Treatment Outcomes with Talazoparib, Romidepsin or Combination in MBL2 cell line

Project description:To explore the molecular mechanisms by which romidepsin potentiates the effect of talazoparib, RNA sequencing analysis of MBL2 cell lines treated with talazoparib, romidepsin, or talazoparib plus romidepsin was performed. 40% of the 2023 genes in combination were from talazoparib, whereas only 5.9% of the genes deregulated during the treatment with the combination of talazoparib plus romidepsin were from the effect of romidepsin. 94 genes were presented in all three treatment groups and included upregulation of Prdm1, Dusp5, and CD74, among others. Analysis of genes responsible for DNA repair, cell cycle arrest and apoptosis demonstrated the contribution of romidepsin to downregulation of DNA repair, the synergistic effect of romidepsin and talazoparib on downregulation of genes of cell cycle leading to cell cycle arrest, and activation of apoptosis by talazoparib predominantly.

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The non-canonical PARP1 inhibitor target, PARP16, contributes to talazoparib polypharmacology and synergy with WEE1 inhibitors: Phosphoproteomics

Project description:PARP1 inhibitors (PARP1is ) display single-agent anticancer activity in small cell lung cancer (SCLC) and other neuroendocrine tumors independent of BRCA1/2 mutations. Here, we determined the differential efficacy of multiple clinical PARP1is in SCLC cells. Compared to the other PARP1is (rucaparib, olaparib and niraparib), talazoparib displayed the highest potency across SCLC, also in SLFN11-negative cells. Chemical proteomics identified PARP16 as a unique talazoparib target in addition to PARP1. Silencing PARP16 significantly reduced cell survival, particularly in combination with PARP1 inhibition. Drug combination screening revealed talazoparib synergy with the WEE1/PLK1 inhibitor, adavosertib. Global phosphoproteomics identified disparate effects on cell cycle and DNA damage response signaling, illustrating underlying mechanisms. Synergy with adavosertib was more pronounced for talazoparib than olaparib and silencing PARP16 further reduced cell survival in combination with olaparib and adavosertib. Together, these data suggest that PARP16 contributes to talazoparib’s overall mechanism of action and constitutes a new actionable target in SCLC.

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The non-canonical PARP1 inhibitor target, PARP16, contributes to talazoparib polypharmacology and synergy with WEE1 inhibitors: Chemical Proteomics

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