Evidence map›Paper›PMID 37554785›Full record

ArticleHeliyon2023

FDX1 inhibits thyroid cancer malignant progression by inducing cuprotosis.

Gaoxiang Chen, Jianan Zhang, Weifeng Teng, Yong Luo, Xiaochun Ji

Abstract read
In one paragraph

Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Role of Ferredoxin 1Cancer pathogenesis and therapy · 2026
    Review
  4. Regulated cell death programs shaping cancer therapy.Cellular oncology (Dordrecht, Netherlands) · 2026
    Review
  5. Article
  6. Cuproptosis and Diabetic Osteoporosis: Mechanisms and Therapeutic Prospects.International journal of molecular sciences · 2026
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. The Role of Cuproptosis Key Factor FDX1 in Gastric Cancer.Current pharmaceutical biotechnology · 2024
    Article
  18. 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

5 authors.

Gaoxiang ChenDepartment of Thyroid and Breast Surgery, Ningbo Medical Center Lihuili Hospital, No.57 XingNing Road, Ningbo, Zhejiang Province, China.
Jianan ZhangDepartment of Thyroid and Breast Surgery, Ningbo Medical Center Lihuili Hospital, No.57 XingNing Road, Ningbo, Zhejiang Province, China.
Weifeng TengDepartment of Thyroid and Breast Surgery, Ningbo Medical Center Lihuili Hospital, No.57 XingNing Road, Ningbo, Zhejiang Province, China.
Yong LuoDepartment of Thyroid and Breast Surgery, Ningbo Medical Center Lihuili Hospital, No.57 XingNing Road, Ningbo, Zhejiang Province, China.
Xiaochun JiDepartment of Thyroid and Breast Surgery, Ningbo Medical Center Lihuili Hospital, No.57 XingNing Road, Ningbo, Zhejiang Province, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cuprotosis is a recently identified cell death form that caused by intracellular copper accumulation and regulated by FDX1. This work aimed to explore the role of cuprotosis and the pivotal regulatory gene FDX1 in thyroid cancer development. We observed that expression of FDX1 in tumor section was notably lower than that in non-tumor sections in clinical samples. Induction of cuprotosis by elesclomol (ES) significantly repressed the in vitro and in vivo growth of thyroid cancer cells, simultaneously elevated Cu level and expression of FDX1, whereas depletion of FDX1 abolished these effects. Knockdown of FDX1 decreased the lipoylation level of DLAT and DLST in thyroid cancer cells, alleviated cuprotosis-induced cell death, simultaneously upregulated the levels of PA and α-KG. These findings demonstrated that FDX1 promotes the cuprotosis of thyroid cancer cells via regulating the lipoylation of DLAT.

Indexed as

CuprotosisDLATFDX1LipoylationThyroid cancer

Identifiers

PMID37554785
PMCPMC10404994

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.