Evidence map›Paper›PMID 38287009›Full record

ArticleCell death & disease2024

AURKA inhibition induces Ewing's sarcoma apoptosis and ferroptosis through NPM1/YAP1 axis.

Huimou Chen, Jing Hu, Xilin Xiong, Hongling Chen, Biaojun Lin, Yusong Chen, Yang Li, Di Cheng, Zhihua Li

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Polyamine Depletion by D,L-α-Difluoromethylornithine Inhibits Ewing Sarcoma Metastasis by Inducing Ferroptosis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  12. KIAA1429 Silencing ameliorates osteosarcoma progression through promoting ferroptosis via Nrf2/NQO1 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

9 authors at 1 institution in 1 country.

Huimou Chen *Department of Oncology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China.
Jing Hu *Department of Clinical Laboratory, The Six Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Xilin Xiong *Department of Oncology, Medical Centre of Pediatric, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Hongling ChenDepartment Of Clinical Laboratory, Maoming People's Hospital, Maoming, Guangdong, People's Republic of China.
Biaojun LinDepartment of Oncology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China.
Yusong ChenDepartment of Oncology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China.
Yang LiDepartment of Oncology, Medical Centre of Pediatric, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China. drliyang@126.com.
Di ChengDepartment of Oncology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China. chengdi@mail.sysu.edu.cn.
Zhihua LiDepartment of Oncology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China. lizhih@mail.sysu.edu.cn.ORCID 0009-0000-0019-4325
Sun Yat-sen University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81672395
6 · The paper itself

Abstract

Ewing's sarcoma (ES) is a rare and highly aggressive malignant tumor arising from bone and soft tissue. Suffering from intractable or recurrent diseases, the patients' therapy options are very limited. It is extremely urgent to identify novel potential therapeutic targets for ES and put them into use in clinical settings. In the present study, high-throughput screening of a small molecular pharmacy library was performed. The killing effect of the Aurora kinase A (AURKA) inhibitor TCS7010 in ES cells was identified, and AURKA was selected as the research object for further study. Disparate suppressants were adopted to study the cell death manner of TCS7010. TCS7010 and RNA silencing were used to evaluate the functions of AURKA in the apoptosis and ferroptosis of ES cells. Co-immunoprecipitation assay was used to investigate the correlation of AURKA and nucleophosmin1 (NPM1) in ES. Nude-mice transplanted tumor model was used for investigating the role of AURKA in ES in vivo. Investigations into the protein activities of AURKA were conducted using ES cell lines and xenograft models. AURKA was found to be prominently upregulated in ES. The AURKA expression level was remarkably connected to ES patients' shorter overall survival (OS) and event-free survival (EFS). Furthermore, AURKA inhibition markedly induced the apoptosis and ferroptosis of ES cells and attenuated tumorigenesis in vivo. On the part of potential mechanisms, it was found that AURKA inhibition triggered the apoptosis and ferroptosis of ES cells through the NPM1/Yes1 associated transcriptional regulator (YAP1) axis, which provides new insights into the tumorigenesis of ES. AURKA may be a prospective target for clinical intervention in ES patients.

Indexed as

FerroptosisSarcoma, EwingAnimalsApoptosisAurora Kinase ACarcinogenesisCell Line, TumorCell Transformation, NeoplasticHumansMiceNuclear ProteinsNucleophosminYAP-Signaling ProteinsAURKA protein, humanAurora Kinase ANPM1 protein, humanNuclear ProteinsNucleophosminYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID38287009
PMCPMC10825207
OpenAlexW4391305259

What OpenQuestion holds

Textmetadata
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.