Evidence map›Paper›PMID 38552003›Full record

ArticleCancer discovery2024

BRCA1-Mediated Dual Regulation of Ferroptosis Exposes a Vulnerability to GPX4 and PARP Co-Inhibition in BRCA1-Deficient Cancers.

Guang Lei, Chao Mao, Amber D Horbath, Yuelong Yan, Shirong Cai, Jun Yao, Yan Jiang, Mingchuang Sun, Xiaoguang Liu, Jun Cheng and 12 more

Open access · greenAbstract read
In one paragraph

Article in Cancer discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
18.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 44 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors at 1 institution in 1 country.

Guang LeiDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-3282-0666
Chao MaoDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-8685-8539
Amber D HorbathDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0003-1482-8637
Yuelong YanDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-8495-6445
Shirong CaiDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-8315-9989
Jun YaoDepartment of Molecular and Cellular Oncology, Division of Basic Sciences, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0003-1418-3576
Yan JiangDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-1945-4200
Mingchuang SunDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-8629-7284
Xiaoguang LiuDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-6977-5128
Jun ChengDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0009-0007-2938-9688
Zhihao XuDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-1593-1962
Hyemin LeeDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-7387-5452
Qidong LiDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-2418-8576
Zhengze LuDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-7703-9224
Li ZhuangDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0009-0009-8355-5274
Mei-Kuang ChenDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-8027-8990
Anagha AlapatiDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0009-0007-2728-5578
Timothy A YapDepartment of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-2154-3309
Mien-Chie HungDepartment of Molecular and Cellular Oncology, Division of Basic Sciences, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0003-4317-4740
Mingjian James YouDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-9111-8068
Helen Piwnica-WormsDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0003-4210-6738
Boyi GanDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-8884-6040
The University of Texas MD Anderson Cancer Center · US

Funding

TRANSLATIONAL AND ANALYTICAL CHEMISTRY COREP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PETER W PISTERS · 1985 to 2026
$279.3M
Tumor hypoxia promotes acquired resistance to radiation through ferroptosis inhibitionU54CA274220 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Steven Hsesheng Lin · 2022 to 2026
$8.4M
Studying metabolic stress signaling in renal cancerR01CA181196 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI GAN, BOYI · 2014 to 2024
$3.4M
Targeting SLC7A11-induced nutrient dependency in cancer: mechanisms and preclinical translationR01CA244144 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI GAN, BOYI · 2020 to 2024
$2.1M
Targeting ferroptosis in cancer therapyR01CA269646 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Boyi Gan · 2023 to 2026
$2.0M
Targeting ferroptosis in radioresistance in lung cancer: mechanisms and preclinical translationR01CA247992 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI GAN, BOYI · 2021 to 2025
$1.9M
Transcriptomic mechanisms underlying the immune modulating function and therapeutic efficacy of PARP inhibitorsR01CA255074 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI YAP, TIMOTHY ANTHONY · 2021 to 2025
$1.8M
Boot Walk Seed Award from Radiation Oncology Strategic Initiatives at The University of Texas MD Anderson Cancer CenterCancer Prevention and Research Institute of Texas (CPRIT) RP220258CPRIT Research Training Award CPRIT Training Program RP210028Institutional Research Fund and Bridge Fund from The University of Texas MD Anderson Cancer CenterNational Institutes of Health (NIH) P30CA016672National Institutes of Health (NIH) R01CA181196National Institutes of Health (NIH) R01CA255074National Science and Technology Council (NSTC) NSTC 112-2639-B-039-001-ASPNCI NIH HHS P30 CA016672NCI NIH HHS R01 CA181196NCI NIH HHS R01 CA244144NCI NIH HHS R01 CA247992NCI NIH HHS R01 CA255074NCI NIH HHS R01 CA269646NCI NIH HHS U54 CA274220Research Center Program from the Ministry of Education in TaiwanThe N.G. and Helen T. Hawkins Distinguished Professorship for Cancer Research of MD Anderson Cancer CenterT-STAR Center NSTC 113-2634-F-039-001U.S. Department of Defense (DOD) W81XWH2210504_BC211174V Foundation VC2020-001
6 · The paper itself

Abstract

Resistance to poly (ADP-ribose) polymerase inhibitors (PARPi) limits the therapeutic efficacy of PARP inhibition in treating breast cancer susceptibility gene 1 (BRCA1)-deficient cancers. Here we reveal that BRCA1 has a dual role in regulating ferroptosis. BRCA1 promotes the transcription of voltage-dependent anion channel 3 (VDAC3) and glutathione peroxidase 4 (GPX4); consequently, BRCA1 deficiency promotes cellular resistance to erastin-induced ferroptosis but sensitizes cancer cells to ferroptosis induced by GPX4 inhibitors (GPX4i). In addition, nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy and defective GPX4 induction unleash potent ferroptosis in BRCA1-deficient cancer cells upon PARPi and GPX4i co-treatment. Finally, we show that xenograft tumors derived from patients with BRCA1-mutant breast cancer with PARPi resistance exhibit decreased GPX4 expression and high sensitivity to PARP and GPX4 co-inhibition. Our results show that BRCA1 deficiency induces a ferroptosis vulnerability to PARP and GPX4 co-inhibition and inform a therapeutic strategy for overcoming PARPi resistance in BRCA1-deficient cancers. Significance: BRCA1 deficiency promotes resistance to erastin-induced ferroptosis via blocking VDAC3 yet renders cancer cells vulnerable to GPX4i-induced ferroptosis via inhibiting GPX4. NCOA4 induction and defective GPX4 further synergizes GPX4i with PARPi to induce ferroptosis in BRCA1-deficient cancers and targeting GPX4 mitigates PARPi resistance in those cancers. See related commentary by Alborzinia and Friedmann Angeli, p. 1372.

Indexed as

BRCA1 ProteinFerroptosisPhospholipid Hydroperoxide Glutathione PeroxidasePoly(ADP-ribose) Polymerase InhibitorsAnimalsBreast NeoplasmsCell Line, TumorFemaleHumansMiceNuclear Receptor CoactivatorsXenograft Model Antitumor AssaysBRCA1 ProteinBRCA1 protein, humanNCOA4 protein, humanNuclear Receptor CoactivatorsPhospholipid Hydroperoxide Glutathione PeroxidasePoly(ADP-ribose) Polymerase Inhibitors

Identifiers

PMID38552003
PMCPMC11296921
OpenAlexW4393319410

What Socratic holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.