Evidence map›Paper›PMID 35127502›Full record

ArticleFrontiers in oncology2021

Deferoxamine Counteracts Cisplatin Resistance in A549 Lung Adenocarcinoma Cells by Increasing Vulnerability to Glutamine Deprivation-Induced Cell Death.

Wen-Jun Liu, Peng-Yu Pan, Ye Sun, Jian-Bo Wang, Huan Zhou, Xin Xie, Zhi-Yuan Duan, Han-Yu Dong, Wen-Na Chen, Li-de Zhang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
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  4. ACTG1 mediates cisplatin resistance in NSCLC through induction of mitochondrial fragmentation.Apoptosis : an international journal on programmed cell death · 2025
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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

11 authors at 2 institutions in 1 country.

Wen-Jun LiuTeaching and Experimental Center, Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Peng-Yu PanDepartment of Cell Biology, College of Integrated Chinese and Western Medical, Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Ye SunKey Laboratory of Environmental Pollution and Microecology of Liaoning Province, Shenyang Medical College, Shenyang, China.
Jian-Bo WangKey Laboratory of Ministry of Education for Traditional Chinese Medicine (TCM) Viscera-State Theory and Applications, Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Huan ZhouDepartment of Cell Biology, College of Integrated Chinese and Western Medical, Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Xin XieTeaching and Experimental Center, Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Zhi-Yuan DuanTeaching and Experimental Center, Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Han-Yu DongDepartment of Cell Biology, College of Integrated Chinese and Western Medical, Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Wen-Na ChenKey Laboratory of Ministry of Education for Traditional Chinese Medicine (TCM) Viscera-State Theory and Applications, Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Li-de ZhangDepartment of Cell Biology, College of Integrated Chinese and Western Medical, Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Chun WangDepartment of Cell Biology, College of Integrated Chinese and Western Medical, Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Liaoning University of Traditional Chinese Medicine · CNShenyang Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glutamine, like glucose, is a major nutrient consumed by cancer cells, yet these cells undergo glutamine starvation in the cores of tumors, forcing them to evolve adaptive metabolic responses. Pharmacologically targeting glutamine metabolism or withdrawal has been exploited for therapeutic purposes, but does not always induce cancer cell death. The mechanism by which cancer cells adapt to resist glutamine starvation in cisplatin-resistant non-small-cell lung cancer (NSCLC) also remains uncertain. Here, we report the potential metabolic vulnerabilities of A549/DDP (drug-resistant human lung adenocarcinoma cell lines) cells, which were more easily killed by the iron chelator deferoxamine (DFO) during glutamine deprivation than their parental cisplatin-sensitive A549 cells. We demonstrate that phenotype resistance to cisplatin is accompanied by adaptive responses during glutamine deprivation partly

Indexed as

cell deathcisplatin resistancedeferoxamineglutamine deprivationmetabolic reprogrammingNSCLC

Identifiers

PMID35127502
PMCPMC8810525
OpenAlexW4206126826

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.