Evidence map›Paper›PMID 41146208›Full record

ReviewCell communication and signaling : CCS2025

SLC7A11 as a bridge between ferroptosis and disulfidptosis: a promising target for tumor treatment.

Hui Qiu, Jing Liu, Nan Shao, Juanjuan Zhao, Chao Chen, Yuanye Jiang, Xu Zhao, Lin Xu

Abstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Review
  2. Review
  3. Disulfidptosis: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. [Role of programmed cell death in platinum resistance in ovarian cancer].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    Review
  13. Article
  14. Review
  15. Review
  16. Ferroptosis-induced immune modulation: a new frontier in glioblastoma therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  17. Review
  18. Review
  19. Article
  20. 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

8 authors.

Hui QiuKey Laboratory of Cancer Prevention & Treatment of Guizhou Province, Zunyi Medical University, Zunyi, Guizhou, 563000, China.
Jing LiuKey Laboratory of Cancer Prevention & Treatment of Guizhou Province, Zunyi Medical University, Zunyi, Guizhou, 563000, China.
Nan ShaoKey Laboratory of Cancer Prevention & Treatment of Guizhou Province, Zunyi Medical University, Zunyi, Guizhou, 563000, China.
Juanjuan ZhaoKey Laboratory of Cancer Prevention & Treatment of Guizhou Province, Zunyi Medical University, Zunyi, Guizhou, 563000, China.
Chao ChenKey Laboratory of Cancer Prevention & Treatment of Guizhou Province, Zunyi Medical University, Zunyi, Guizhou, 563000, China.
Yuanye JiangDepartment of Gastroenterology, Putuo hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200062, China. yuanye1014@126.com.
Xu ZhaoKey Laboratory of Cancer Prevention & Treatment of Guizhou Province, Zunyi Medical University, Zunyi, Guizhou, 563000, China. zhaoxu07122021@163.com.
Lin XuKey Laboratory of Cancer Prevention & Treatment of Guizhou Province, Zunyi Medical University, Zunyi, Guizhou, 563000, China. xulinzhouya@163.com.

Funding

The National Natural Science Foundation of China 82160503
6 · The paper itself

Abstract

Cell death is a basic physiological process involved in embryonic development, aging, immune responses and other life processes. In particular, ferroptosis and disulfidptosis are two forms of regulatory cell death (RCD) that have been identified in recent years as being caused by imbalances in cellular metabolism. Solute Carrier Family 7 Member 11 (SLC7A11, xCT), a cystine transporter, is often highly expressed in tumor cells, which not only participates in the synthesis of glutathione (GSH), but also plays an indispensable role in the inhibition of oxidative stress-induced ferroptosis. However, glucose starvation of SLC7A11 high tumor cells consumes a large amount of NADPH, leading to disulfide stress in actin cytoskeletal proteins, which triggers disulfidptosis. These findings suggest that there is an intrinsic relationship between ferroptosis and disulfidptosis and that SLC7A11 connects the regulation of both forms of death. In this article, we first reviewed the regulatory mechanism controlling SLC7A11 expression and its function and then focused on its role and mechanism in mediating ferroptosis and disulfidptosis in tumorigenesis and treatment. Finally, we carefully discussed the intrinsic links between ferroptosis and disulfidptosis as well as the remaining scientific issues related to their mediation of tumorigenesis and treatment, aiming to provide a new perspective for cancer treatment, especially in the development of strategies for targeted treatment against specific metabolic pathways.

Indexed as

Amino Acid Transport System y+DisulfidptosisFerroptosisNeoplasmsAnimalsHumansAmino Acid Transport System y+SLC7A11 protein, humanDisulfidptosisFerroptosisMetabolismSLC7A11Tumor

Identifiers

PMID41146208
PMCPMC12557889

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.