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Combined inhibition of topoisomerase I and poly(ADP-ribose) polymerase: A synergistic therapeutic strategy for glioblastoma with phosphatase and tensin homolog deficiency

Title: Combined inhibition of topoisomerase I and poly(ADP-ribose) polymerase: A synergistic therapeutic strategy for glioblastoma with phosphatase and tensin homolog deficiency
Authors: Kim, Olga; Butler, Madison; Sergi, Zach; Robey, Robert W; Zhang, Meili; Chari, Raj; Pang, Ying; Yu, Guangyang; Zhang, Wei; Song, Hua; Davis, Dionne; Hawley, Robert G; Wen, Xinyu; Wang, Herui; Quezado, Martha; Tran, Bao; Merchant, Mythili; Ranjan, Alice; Furnari, Frank B; Khan, Javed; Gilbert, Mark R; Ryan Miller, Christopher; Gottesman, Michael M; Pommier, Yves; Wu, Jing
Contributors: National Institutes of Health; Lasker Clinical Research
Source: Neuro-Oncology Advances ; volume 5, issue 1 ; ISSN 2632-2498
Publisher Information: Oxford University Press (OUP)
Publication Year: 2023
Description: Background Deletions or loss-of-function mutations in phosphatase and tensin homolog (PTEN) are common in glioblastoma (GBM) and have been associated with defective DNA damage repair. Here we investigated whether PTEN deficiency presents a vulnerability to a simultaneous induction of DNA damage and suppression of repair mechanisms by combining topoisomerase I (TOP1) and PARP inhibitors. Methods Patient-derived GBM cells and isogenic PTEN-null and PTEN-WT glioma cells were treated with LMP400 (Indotecan), a novel non-camptothecin TOP1 inhibitor alone and in combination with a PARP inhibitor, Olaparib or Niraparib. RNAseq analysis was performed to identify treatment-induced dysregulated pathways. Results We found that GBM cells lacking PTEN expression are highly sensitive to LMP400; however, rescue of the PTEN expression reduces sensitivity to the treatment. Combining LMP400 with Niraparib leads to synergistic cytotoxicity by inducing G2/M arrest, DNA damage, suppression of homologous recombination-related proteins, and activation of caspase 3/7 activity significantly more in PTEN-null cells compared to PTEN-WT cells. LMP400 and Niraparib are not affected by ABCB1 and ABCG2, the major ATP-Binding Cassette (ABC) drug efflux transporters expressed at the blood-brain barrier (BBB), thus suggesting BBB penetration which is a prerequisite for potential brain tumor treatment. Animal studies confirmed both an anti-glioma effect and sufficient BBB penetration to prolong survival of mice treated with the drug combination. Conclusions Our findings provide a proof of concept for the combined treatment with LMP400 and Niraparib in a subset of GBM patients with PTEN deficiency.
Document Type: article in journal/newspaper
Language: English
DOI: 10.1093/noajnl/vdad102
DOI: 10.1093/noajnl/vdad102/51176613/vdad102.pdf
Availability: https://doi.org/10.1093/noajnl/vdad102; https://academic.oup.com/noa/advance-article-pdf/doi/10.1093/noajnl/vdad102/51176613/vdad102.pdf; https://academic.oup.com/noa/article-pdf/5/1/vdad102/51531730/vdad102.pdf
Accession Number: edsbas.40940D80
Database: BASE