Evidence map›Paper›PMID 39345091›Full record

ArticleCancer biology & therapy2024

FASN contributes to ADM resistance of diffuse large B-cell lymphoma by inhibiting ferroptosis via nf-κB/STAT3/GPX4 axis.

Xing Zhong, Weiwei Zhang, Weiming Zhang, Nasha Yu, Wuping Li, Xiangxiang Song

Abstract read
In one paragraph

Article in Cancer biology & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–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

16 citing papers in PubMed.

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  14. Synergistic effects of dihydroartemisinin and cisplatin on inducing ferroptosis in gastric cancer through GPX4 inhibition.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025
    Article
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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

6 authors.

Xing ZhongDepartments of Lymphatic and Hematological Oncology, Jiangxi Cancer Hospital (The Second Affiliated Hospital of Nanchang Medical College), Nanchang, Jiangxi, P. R. China.
Weiwei ZhangJXHC Key Laboratory of Tumor Microenvironment and Immunoregulation (Jiangxi Cancer Hospital), Nanchang, Jiangxi, P. R. China.
Weiming ZhangNanchang Medical College, Nanchang, Jiangxi, P. R. China.
Nasha YuDepartments of Lymphatic and Hematological Oncology, Jiangxi Cancer Hospital (The Second Affiliated Hospital of Nanchang Medical College), Nanchang, Jiangxi, P. R. China.
Wuping LiDepartments of Lymphatic and Hematological Oncology, Jiangxi Cancer Hospital (The Second Affiliated Hospital of Nanchang Medical College), Nanchang, Jiangxi, P. R. China.
Xiangxiang SongDepartments of Lymphatic and Hematological Oncology, Jiangxi Cancer Hospital (The Second Affiliated Hospital of Nanchang Medical College), Nanchang, Jiangxi, P. R. China.ORCID 0009-0001-0226-7513

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug resistance is a critical impediment to efficient therapy of diffuse large B-cell lymphoma (DLBCL) patients. Recent studies have highlighted the association between ferroptosis and drug resistance that has been reported. Fatty acid synthase (FASN) is always related to a poor prognosis. In this study, we investigate the impact of FASN on drug resistance in DLBCL and explore its potential modulation of ferroptosis mechanisms. The clinical correlation of FASN mRNA expression was first analyzed to confirm the role of FASN on drug resistance in DLBCL based on the TCGA database. Next, the impact of FASN on ferroptosis was investigated in vitro and in vivo. Furthermore, a combination of RNA-seq, western blot, luciferase reporter, and ChIP experiments was employed to elucidate the underlying mechanism. The prognosis for patients with DLBCL was worse when FASN was highly expressed, particularly in those undergoing chemotherapy for Adriamycin (ADM). FASN promoted tumor growth and resistance of DLBCL to ADM, both in vitro and in vivo. It is noteworthy that this effect was achieved by inhibiting ferroptosis, since Fer-1 (a ferroptosis inhibitor) treatment significantly recovered the effects of silencing FASN on inhibiting ferroptosis, while Erastin (a ferroptosis inducer) treatment attenuated the impact of overexpressing FASN. Mechanistically, FASN activated NF-κB/STAT3 signaling pathway through phosphorylating the upstream IKKα and IκBα, and the activated STAT3 promoted GPX4 expression by directly binding to GPX4 promoter. FASN inhibits ferroptosis in DLBCL via NF-κB/STAT3/GPX4 signaling pathway, indicating its critical role in mediating ADM resistance of DLBCL.

Indexed as

DoxorubicinDrug Resistance, NeoplasmFatty Acid Synthase, Type IFerroptosisLymphoma, Large B-Cell, DiffuseAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeNF-kappa BPhospholipid Hydroperoxide Glutathione PeroxidasePrognosisDoxorubicinFASN protein, humanFatty Acid Synthase, Type INF-kappa BPhospholipid Hydroperoxide Glutathione PeroxidaseSTAT3 protein, humanSTAT3 Transcription FactorDLBCLdrug resistanceFASNferroptosisNf-κB/STAT3/GPX4 axis

Identifiers

PMID39345091
PMCPMC11445901

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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.