Mitochondrial NADP(H)–dependent de novo dTMP biosynthesis counteracts the cytotoxicity of PARP inhibitors

PARP inhibitors (PARPis), known to elicit mitochondrial protection in nononcological diseases by elevating the cellular NAD + pool, exhibit potent cytotoxicity in selected human cancers. The role of mitochondrial metabolism in PARPi-mediated antitumor therapy remains unexplored. Here, we propose a causal link between mitochondrial NAD + metabolism and PARPi responsiveness. In PARPi-non-responsive tumor cells, PARP inhibition specifically expands mitochondrial NADP(H) [mito-NADP(H)] pool, thereby facilitating de novo mitochondrial dTMP (mito-dTMP) biosynthesis and maintaining mitochondrial dTTP (mito-dTTP) pool to prevent uracil misincorporation into mitochondrial DNA (mtDNA), regardless of homologous recombination (HR) status. Mechanistically, loss of PTPN1 ADPRylation by PARPi abolishes its phosphatase activity toward STAT3, yielding enhanced STAT3 phosphorylation and the subsequent transactivation of FoxO1. FoxO1 modulates transcriptomic signature governing mitochondrial NADPH fluxes to de novo mito-dTMP generation. Our results uncover a fundamental vulnerability that can be leveraged by cotargeting STAT3 and PARP to trigger mitochondrial dysfunction.

Authors

Institutions

Publication Details

Journal
Proceedings of the National Academy of Sciences
Published
2026-09-24
DOI
https://doi.org/10.1073/pnas.2607452123
Primary Topic
PARP inhibition in cancer therapy
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
article

Mitochondrial NADP(H)–dependent de novo dTMP biosynthesis counteracts the cytotoxicity of PARP inhibitors

Han Wook You, Xianming Deng, Xiaoniu He, Fan Gao et al.
Proceedings of the National Academy of Sciences
PARP inhibition in cancer therapy
article

Mitochondrial NADP(H)–dependent de novo dTMP biosynthesis counteracts the cytotoxicity of PARP inhibitors

Han Wook You, Xianming Deng, Xiaoniu He, Fan Gao, Hong Zheng, Canhua Huang, Wenbin Lu, Wen Liu, Chen Liu, Chensong Zhang, Yuanpei Li, Tong Shu, Pingping Liu, Zhenyu Yin, Min Zheng, Qing Li, Lei Zhang, Huiwen Zhang, Jing Ye
article en

Abstract

PARP inhibitors (PARPis), known to elicit mitochondrial protection in nononcological diseases by elevating the cellular NAD + pool, exhibit potent cytotoxicity in selected human cancers. The role of mitochondrial metabolism in PARPi-mediated antitumor therapy remains unexplored. Here, we propose a causal link between mitochondrial NAD + metabolism and PARPi responsiveness. In PARPi-non-responsive tumor cells, PARP inhibition specifically expands mitochondrial NADP(H) [mito-NADP(H)] pool, thereby facilitating de novo mitochondrial dTMP (mito-dTMP) biosynthesis and maintaining mitochondrial dTTP (mito-dTTP) pool to prevent uracil misincorporation into mitochondrial DNA (mtDNA), regardless of homologous recombination (HR) status. Mechanistically, loss of PTPN1 ADPRylation by PARPi abolishes its phosphatase activity toward STAT3, yielding enhanced STAT3 phosphorylation and the subsequent transactivation of FoxO1. FoxO1 modulates transcriptomic signature governing mitochondrial NADPH fluxes to de novo mito-dTMP generation. Our results uncover a fundamental vulnerability that can be leveraged by cotargeting STAT3 and PARP to trigger mitochondrial dysfunction.

Proceedings of the National Academy of SciencesVol. 123(39)
Sun Yat-sen University (CN), Xiamen University (CN), Sichuan University (CN), Zhongshan Hospital of Xiamen University (CN), Sun Yat-sen University Cancer Center (CN), Ministry of Education (ET), Xijing Hospital (CN), Air Force Medical University (CN)
Good health and well-being
Openalex Percentile: Top 14%
PARP inhibition in cancer therapy
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.