Evidence map›Paper›PMID 39009982›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

The dual role of FSP1 in programmed cell death: resisting ferroptosis in the cell membrane and promoting necroptosis in the nucleus of THP-1 cells.

Xiaoqian Tan, Yinling He, Panpan Yu, Yunong Deng, Zhongcheng Xie, Jiami Guo, Qin Hou, Pin Li, Xiaoyan Lin, Siyu Ouyang and 14 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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  5. Article
  6. Review
  7. Article
  8. Review
  9. Molecular principles underlying aggressive cancers.Signal transduction and targeted therapy · 2025
    Review
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

24 authors.

Xiaoqian Tan *Department of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Yinling He *Department of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Panpan Yu *Department of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Yunong Deng *Department of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Zhongcheng XieDepartment of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Jiami GuoDepartment of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Qin HouDepartment of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Pin LiDepartment of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Xiaoyan LinDepartment of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Siyu OuyangDepartment of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Wentao MaDepartment of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Yushu XieClass of Clinical Medicine, University of South China, Hengyang, 421001, Hunan, China.
Zilong GuoClass of Clinical Medicine, University of South China, Hengyang, 421001, Hunan, China.
Dandan ChenClass of Clinical Medicine, University of South China, Hengyang, 421001, Hunan, China.
Zhixia ZhangClass of Clinical Medicine, University of South China, Hengyang, 421001, Hunan, China.
Yunyu ZhuClass of Clinical Medicine, University of South China, Hengyang, 421001, Hunan, China.
Fei HuangClass of Clinical Medicine, University of South China, Hengyang, 421001, Hunan, China.
Ziye ZhaoClass of Clinical Medicine, University of South China, Hengyang, 421001, Hunan, China.
Cen ZhangClass of Clinical Medicine, University of South China, Hengyang, 421001, Hunan, China.
Zhirong GuoClass of Clinical Medicine, University of South China, Hengyang, 421001, Hunan, China.
Xi ChenDepartment of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Tianhong PengDepartment of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China. 2602406228@qq.com.
Liang LiDepartment of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China. 26002860@qq.com.
Wei XieDepartment of Physiology, Clinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China. weixiehy@126.com.

Funding

College Students' Research Learning and Innovative Experiment Plan in University of South China 202110555098College Students' Research Learning and Innovative Experiment Plan in University of South China 2022X10555115College Students' Research Learning and Innovative Experiment Plan in University of South China S202110555307College Students' Research Learning and Innovative Experiment Plan in University of South China S202210555256College Students' Research Learning and Innovative Experiment Plan in University of South China X202110555516College Students' Research Learning and Innovative Experiment Plan in University of South China X202110555523College Students' Research Learning and Innovative Experiment Plan in University of South China X202110555529the financial supports from the science and technology plan project of Hengyang City 202150063459the financial supports from the scientific research project of health commission of Hunan province 202101021784the Hunan Provincial Natural Science Foundation of China 2021JJ30020the National Natural Sciences Foundation of China 81800386
6 · The paper itself

Abstract

backgroundAcute monocytic leukemia-M5 (AML-M5) remains a challenging disease due to its high morbidity and poor prognosis. In addition to the evidence mentioned earlier, several studies have shown that programmed cell death (PCD) serves a critical function in treatment of AML-M5. However, the role and relationship between ferroptosis and necroptosis in AML-M5 remains unclear.

methodsTHP-1 cells were mainly treated with Erastin and IMP-366. The changes of ferroptosis and necroptosis levels were detected by CCK-8, western blot, quantitative real-time PCR, and electron microscopy. Flow cytometry was applied to detect the ROS and lipid ROS levels. MDA, 4-HNE, GSH and GSSG were assessed by ELISA kits. Intracellular distribution of FSP1 was studied by immunofluorescent staining and western blot.

resultsThe addition of the myristoylation inhibitor IMP-366 to erastin-treated acute monocytic leukemia cell line THP-1 cell not only resulted in greater susceptibility to ferroptosis characterized by lipid peroxidation, glutathione (GSH) depletion and mitochondrial shrinkage, as the FSP1 position on membrane was inhibited, but also increased p-RIPK1 and p-MLKL protein expression, as well as a decrease in caspase-8 expression, and triggered the characteristic necroptosis phenomena, including cytoplasmic translucency, mitochondrial swelling, membranous fractures by FSP1 migration into the nucleus via binding importin α2. It is interesting to note that ferroptosis inhibitor fer-1 reversed necroptosis.

conclusionWe demonstrated that inhibition of myristoylation by IMP-366 is capable of switching ferroptosis and ferroptosis-dependent necroptosis in THP-1 cells. In these findings, FSP1-mediated ferroptosis and necroptosis are described as alternative mechanisms of PCD of THP-1 cells, providing potential therapeutic strategies and targets for AML-M5.

Indexed as

FerroptosisNecroptosisAcrylamidesApoptosisCell MembraneCell NucleusHumansNuclear Pore Complex ProteinsPiperazinesReactive Oxygen SpeciesRNA-Binding ProteinsS100 Calcium-Binding Protein A4SulfonamidesTHP-1 CellsAcrylamidesAGFG1 protein, humanerastinN-(4-(N-(3-methoxypyrazin-2-yl)sulfamoyl)phenyl)-3-(5-nitrothiophene-2-yl)acrylamideNuclear Pore Complex ProteinsPiperazinesReactive Oxygen SpeciesRNA-Binding ProteinsS100A4 protein, humanS100 Calcium-Binding Protein A4SulfonamidesAML-M5FerroptosisFSP1MyristoylationNecroptosisTHP-1 cells

Identifiers

PMID39009982
PMCPMC11247902

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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.