Metabolic dependency mapping identifies Peroxiredoxin 1 as a driver of resistance to ATM inhibition

Metabolic pathways fuel tumor progression and resistance to stress conditions including chemotherapeutic drugs, such as DNA damage response (DDR) inhibitors. Yet, significant gaps persist in how metabolic pathways confer resistance to DDR inhibition in cancer cells. Here, we employed a metabolism-fo...

Full description

Saved in:
Bibliographic Details
Main Authors: Haojian Li, Takashi Furusawa, Renzo Cavero, Yunjie Xiao, Raj Chari, Xiaolin Wu, David Sun, Oliver Hartmann, Anjali Dhall, Ronald Holewinski, Thorkell Andresson, Baktiar Karim, Marina Villamor-Payà, Devorah Gallardo, Chi-Ping Day, Lipika R. Pal, Nishanth Ulhas Nair, Eytan Ruppin, Mirit I. Aladjem, Yves Pommier, Markus E. Diefenbacher, Jung Mi Lim, Rodney L. Levine, Travis H. Stracker, Urbain Weyemi
Format: Article
Language:English
Published: Elsevier 2025-03-01
Series:Redox Biology
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2213231725000163
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849720594145214464
author Haojian Li
Takashi Furusawa
Renzo Cavero
Yunjie Xiao
Raj Chari
Xiaolin Wu
David Sun
Oliver Hartmann
Anjali Dhall
Ronald Holewinski
Thorkell Andresson
Baktiar Karim
Marina Villamor-Payà
Devorah Gallardo
Chi-Ping Day
Lipika R. Pal
Nishanth Ulhas Nair
Eytan Ruppin
Mirit I. Aladjem
Yves Pommier
Markus E. Diefenbacher
Jung Mi Lim
Rodney L. Levine
Travis H. Stracker
Urbain Weyemi
author_facet Haojian Li
Takashi Furusawa
Renzo Cavero
Yunjie Xiao
Raj Chari
Xiaolin Wu
David Sun
Oliver Hartmann
Anjali Dhall
Ronald Holewinski
Thorkell Andresson
Baktiar Karim
Marina Villamor-Payà
Devorah Gallardo
Chi-Ping Day
Lipika R. Pal
Nishanth Ulhas Nair
Eytan Ruppin
Mirit I. Aladjem
Yves Pommier
Markus E. Diefenbacher
Jung Mi Lim
Rodney L. Levine
Travis H. Stracker
Urbain Weyemi
author_sort Haojian Li
collection DOAJ
description Metabolic pathways fuel tumor progression and resistance to stress conditions including chemotherapeutic drugs, such as DNA damage response (DDR) inhibitors. Yet, significant gaps persist in how metabolic pathways confer resistance to DDR inhibition in cancer cells. Here, we employed a metabolism-focused CRISPR knockout screen and identified genetic vulnerabilities to DDR inhibitors. We unveiled Peroxiredoxin 1 (PRDX1) as a synthetic lethality partner with Ataxia Telangiectasia Mutated (ATM) kinase. Tumor cells depleted of PRDX1 displayed heightened sensitivity to ATM inhibition in vitro and in mice in a manner dependent on p53 status. Mechanistically, we discovered that the ribosomal protein RPL32 undergoes redox modification on active cysteine residues 91 and 96 upon ATM inhibition, promoting p53 stability and altered cell fitness. Our findings reveal a new pathway whereby RPL32 senses stress and induces p53 activation impairing tumor cell survival.
format Article
id doaj-art-1c7e9e211cd047cebe94db05a8c2e5a8
institution DOAJ
issn 2213-2317
language English
publishDate 2025-03-01
publisher Elsevier
record_format Article
series Redox Biology
spelling doaj-art-1c7e9e211cd047cebe94db05a8c2e5a82025-08-20T03:11:54ZengElsevierRedox Biology2213-23172025-03-018010350310.1016/j.redox.2025.103503Metabolic dependency mapping identifies Peroxiredoxin 1 as a driver of resistance to ATM inhibitionHaojian Li0Takashi Furusawa1Renzo Cavero2Yunjie Xiao3Raj Chari4Xiaolin Wu5David Sun6Oliver Hartmann7Anjali Dhall8Ronald Holewinski9Thorkell Andresson10Baktiar Karim11Marina Villamor-Payà12Devorah Gallardo13Chi-Ping Day14Lipika R. Pal15Nishanth Ulhas Nair16Eytan Ruppin17Mirit I. Aladjem18Yves Pommier19Markus E. Diefenbacher20Jung Mi Lim21Rodney L. Levine22Travis H. Stracker23Urbain Weyemi24Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute/National Institutes of Health, 37 Convent Drive, Bethesda, MD, 20892, USA; Department of Molecular Biosciences, The University of Texas at Austin, Austin, TX, 78712, USADevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute/National Institutes of Health, 37 Convent Drive, Bethesda, MD, 20892, USADevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute/National Institutes of Health, 37 Convent Drive, Bethesda, MD, 20892, USADevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute/National Institutes of Health, 37 Convent Drive, Bethesda, MD, 20892, USAGenome Modification Core, Laboratory Animal Sciences Program, Frederick, MD, USANCI Genomics Technology Laboratory, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research/ Frederick, Maryland, USANCI Genomics Technology Laboratory, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research/ Frederick, Maryland, USAComprehensive Pneumology Center (CPC)/Institute of Lung Health and Immunity (LHI), Helmholtz Munich, Member of the German Center for Lung Research (DZL/CPC-M), Munich, GermanyDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute/National Institutes of Health, 37 Convent Drive, Bethesda, MD, 20892, USAProtein Characterization Laboratory/Cancer Research Technology Program/Frederick National Laboratory for Cancer Research, Frederick, MD, USAProtein Characterization Laboratory/Cancer Research Technology Program/Frederick National Laboratory for Cancer Research, Frederick, MD, USAMolecular Histopathology Laboratory/ Cancer Research Technology Program/Frederick National Laboratory for Cancer Research/ Frederick, Maryland, USARadiation Oncology Branch/CCR/NCI, USALaboratory Animal Sciences Program, Leidos Biomedical Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USACancer Data Science Lab/ Center for Cancer Research/National Cancer Institute/National Institutes of Health, Bethesda, MD, 20892, USACancer Data Science Lab/ Center for Cancer Research/National Cancer Institute/National Institutes of Health, Bethesda, MD, 20892, USACancer Data Science Lab/ Center for Cancer Research/National Cancer Institute/National Institutes of Health, Bethesda, MD, 20892, USACancer Data Science Lab/ Center for Cancer Research/National Cancer Institute/National Institutes of Health, Bethesda, MD, 20892, USADevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute/National Institutes of Health, 37 Convent Drive, Bethesda, MD, 20892, USADevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute/National Institutes of Health, 37 Convent Drive, Bethesda, MD, 20892, USAComprehensive Pneumology Center (CPC)/Institute of Lung Health and Immunity (LHI), Helmholtz Munich, Member of the German Center for Lung Research (DZL/CPC-M), Munich, GermanyLaboratory of Biochemistry, National Heart, Lung, and Blood Institute, Bethesda, MD, USALaboratory of Biochemistry, National Heart, Lung, and Blood Institute, Bethesda, MD, USARadiation Oncology Branch/CCR/NCI, USADevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute/National Institutes of Health, 37 Convent Drive, Bethesda, MD, 20892, USA; Corresponding author. Developmental Therapeutics Branch National Cancer Institute, National Institutes of Health 37 Convent Drive, Bethesda, MD, 20892, USA.Metabolic pathways fuel tumor progression and resistance to stress conditions including chemotherapeutic drugs, such as DNA damage response (DDR) inhibitors. Yet, significant gaps persist in how metabolic pathways confer resistance to DDR inhibition in cancer cells. Here, we employed a metabolism-focused CRISPR knockout screen and identified genetic vulnerabilities to DDR inhibitors. We unveiled Peroxiredoxin 1 (PRDX1) as a synthetic lethality partner with Ataxia Telangiectasia Mutated (ATM) kinase. Tumor cells depleted of PRDX1 displayed heightened sensitivity to ATM inhibition in vitro and in mice in a manner dependent on p53 status. Mechanistically, we discovered that the ribosomal protein RPL32 undergoes redox modification on active cysteine residues 91 and 96 upon ATM inhibition, promoting p53 stability and altered cell fitness. Our findings reveal a new pathway whereby RPL32 senses stress and induces p53 activation impairing tumor cell survival.http://www.sciencedirect.com/science/article/pii/S2213231725000163ATM kinasePeroxiredoxin 1Disulfide stressp53 activationRPL32 redox modification
spellingShingle Haojian Li
Takashi Furusawa
Renzo Cavero
Yunjie Xiao
Raj Chari
Xiaolin Wu
David Sun
Oliver Hartmann
Anjali Dhall
Ronald Holewinski
Thorkell Andresson
Baktiar Karim
Marina Villamor-Payà
Devorah Gallardo
Chi-Ping Day
Lipika R. Pal
Nishanth Ulhas Nair
Eytan Ruppin
Mirit I. Aladjem
Yves Pommier
Markus E. Diefenbacher
Jung Mi Lim
Rodney L. Levine
Travis H. Stracker
Urbain Weyemi
Metabolic dependency mapping identifies Peroxiredoxin 1 as a driver of resistance to ATM inhibition
Redox Biology
ATM kinase
Peroxiredoxin 1
Disulfide stress
p53 activation
RPL32 redox modification
title Metabolic dependency mapping identifies Peroxiredoxin 1 as a driver of resistance to ATM inhibition
title_full Metabolic dependency mapping identifies Peroxiredoxin 1 as a driver of resistance to ATM inhibition
title_fullStr Metabolic dependency mapping identifies Peroxiredoxin 1 as a driver of resistance to ATM inhibition
title_full_unstemmed Metabolic dependency mapping identifies Peroxiredoxin 1 as a driver of resistance to ATM inhibition
title_short Metabolic dependency mapping identifies Peroxiredoxin 1 as a driver of resistance to ATM inhibition
title_sort metabolic dependency mapping identifies peroxiredoxin 1 as a driver of resistance to atm inhibition
topic ATM kinase
Peroxiredoxin 1
Disulfide stress
p53 activation
RPL32 redox modification
url http://www.sciencedirect.com/science/article/pii/S2213231725000163
work_keys_str_mv AT haojianli metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT takashifurusawa metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT renzocavero metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT yunjiexiao metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT rajchari metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT xiaolinwu metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT davidsun metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT oliverhartmann metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT anjalidhall metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT ronaldholewinski metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT thorkellandresson metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT baktiarkarim metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT marinavillamorpaya metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT devorahgallardo metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT chipingday metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT lipikarpal metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT nishanthulhasnair metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT eytanruppin metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT miritialadjem metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT yvespommier metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT markusediefenbacher metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT jungmilim metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT rodneyllevine metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT travishstracker metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition
AT urbainweyemi metabolicdependencymappingidentifiesperoxiredoxin1asadriverofresistancetoatminhibition