Evidence map›Paper›PMID 40022222›Full record

ArticleJournal of translational medicine2025

Cancer-associated fibroblasts promote doxorubicin resistance in triple-negative breast cancer through enhancing ZFP64 histone lactylation to regulate ferroptosis.

KeJing Zhang, Lei Guo, Xin Li, Yu Hu, Na Luo

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Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

53 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  5. P53 Competitively Binds P300 to Suppress HIF-1α/TFRC-Mediated Ferroptosis and Promote Doxorubicin Resistance in Breast Cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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

5 authors.

KeJing ZhangDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan Province, 410008, P.R. China.
Lei GuoDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan Province, 410008, P.R. China.
Xin LiDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan Province, 410008, P.R. China.
Yu HuDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan Province, 410008, P.R. China.
Na LuoDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan Province, 410008, P.R. China. luonaxy2012@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCancer-associated fibroblasts (CAFs) have been identified to drive chemotherapy resistance in triple-negative breast cancer (TNBC). This study evaluated the functions of CAFs-mediated suppressive ferroptosis in doxorubicin (DOX) resistance in TNBC and its detailed molecular mechanisms.

methodsTNBC cell lines were co-cultured with CAFs isolated from DOX-sensitive (CAF/S) or DOX-resistant (CAF/R) breast cancer tissues. Cell viability and death were assessed by cell counting Kit-8 (CCK-8) and propidium iodide (PI) staining. Ferroptosis was evaluated by detection of Fe

resultsCAFs-derived lactate repressed ferroptosis to confer resistance of TNBC cells to DOX. Moreover, zinc finger protein 64 (ZFP64) expression was elevated in DOX-resistant TNBC and was associated with high histone lactylation level. CAFs facilitated histone lactylation to enhance ZFP64 expression, which triggered ferroptosis inhibition and DOX resistance. In addition, ZFP64 bound to the promoters of GTP cyclohydrolase-1 (GCH1) and ferritin heavy chain 1 (FTH1), thereby promoting their expression. Rescue experiments indicated that ZFP64 silencing-induced ferroptosis and high sensitivity of TNBC cells to DOX could be counteracted by GCH1 or FTH1 overexpression.

conclusionCAFs acted as a ferroptosis inhibitor to cause DOX resistance of TNBC via histone lactylation-mediated ZFP64 up-regulation and subsequent promotion of GCH1-induced lipid peroxidation inhibition and FTH1-induced intracellular Fe

Indexed as

Cancer-Associated FibroblastsDoxorubicinDrug Resistance, NeoplasmFerroptosisHistonesTranscription FactorsTriple Negative Breast NeoplasmsAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMiceMice, NudeReactive Oxygen SpeciesThyroid Hormone-Binding ProteinsDoxorubicinHistonesReactive Oxygen SpeciesThyroid Hormone-Binding ProteinsTranscription FactorsCAFsDOX resistanceFerroptosisHistone lactylationTNBCZFP64

Identifiers

PMID40022222
PMCPMC11871786

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Registered trials

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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 OpenQuestion graph.