Evidence map›Paper›PMID 39739602›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Inhibition of Endoplasmic Reticulum Stress Cooperates with SLC7A11 to Promote Disulfidptosis and Suppress Tumor Growth upon Glucose Limitation.

Jin Wang, Jing Chen, Kexin Fan, Minglin Wang, Min Gao, Yakun Ren, Shaobo Wu, Qian He, Kangsheng Tu, Qiuran Xu and 1 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed.

  1. Review
  2. Disulfidptosis: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Regulated cell death programs shaping cancer therapy.Cellular oncology (Dordrecht, Netherlands) · 2026
    Review
  11. [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
  12. Review
  13. Article
  14. Review
  15. Article
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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.

Jin WangDepartment of Hepatobiliary Surgery, the First Affiliated Hospital, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.
Jing ChenShaanxi Stem Cell Engineering Application Research Center, Shaanxi Jiuzhou Biomedical Science and Technology Group, Xi'an, Shaanxi, 710065, China.
Kexin FanDepartment of Hepatobiliary Surgery, the First Affiliated Hospital, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.
Minglin WangDepartment of Hepatobiliary Surgery, the First Affiliated Hospital, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.
Min GaoDepartment of Hepatobiliary Surgery, the First Affiliated Hospital, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.
Yakun RenDepartment of Hepatobiliary Surgery, the First Affiliated Hospital, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.
Shaobo WuDepartment of Hepatobiliary Surgery, the First Affiliated Hospital, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.
Qian HeDepartment of Hepatobiliary Surgery, the First Affiliated Hospital, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.
Kangsheng TuDepartment of Hepatobiliary Surgery, the First Affiliated Hospital, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.
Qiuran XuZhejiang Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine, Hangzhou Medical College, Hangzhou, Zhejiang, 311300, China.
Yilei ZhangDepartment of Hepatobiliary Surgery, the First Affiliated Hospital, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.ORCID https://orcid.org/0000-0003-1407-0301

Funding

Department of Science and Technology of Shaanxi Province, China 2022KW-48Department of Science and Technology of Shaanxi Province, China 2024JC-TBZC-13Department of Science and Technology of Shaanxi Province, China QCYRCXM-2022-142Department of Science and Technology of Shaanxi Province, China QCYRCXM-2022-166National Natural Science Foundation of China 82103272National Natural Science Foundation of China 82372847Natural Science Foundation of Zhejiang Province LR22H160008Science and Technology Department of Zhejiang Province 2024C02G1361923
6 · The paper itself

Abstract

Disulfidptosis is a newly discovered type of regulated cell death triggered by disulfide bond accumulation and NADPH (nicotinamide adenine dinucleotide phosphate) depletion due to glucose deprivation. However, the regulatory mechanisms involving additional cellular circuits remain unclear. Excessive disulfide bond accumulation can impair endoplasmic reticulum (ER) homeostasis and activate the ER stress response. In this study, we found that SLC7A11-mediated disulfidptosis upon glucose deprivation is accompanied by ER stress induction. Pharmacological inhibition of SLC7A11-mediated cystine uptake or cystine withdrawal not only blocks disulfidptosis under glucose starvation but also suppresses the ER stress response, indicating a close link between these processes. Moreover, inhibitors targeting the ER stress response promote disulfidptosis, while ER stress inducers suppress glucose starvation-induced disulfidptosis in SLC7A11-high-expressing cells, suggesting a protective role for ER stress during disulfidptosis. Similar effects are observed in cells treated with glucose transporter inhibitors (GLUTi). Finally, combined treatment with ER stress inhibitors and GLUTi significantly suppresses tumor growth both in vitro and in vivo by inducing disulfide stress and subsequent disulfidptosis. In summary, these findings reveal a novel role for ER stress in regulating disulfidptosis and provide theoretical insights into the potential application of GLUTi and ER stress inhibitors in cancer therapy.

Indexed as

Amino Acid Transport System y+Endoplasmic Reticulum StressGlucoseNeoplasmsAnimalsApoptosisCell Line, TumorCell ProliferationDisulfidptosisHumansMiceAmino Acid Transport System y+GlucoseSLC7A11 protein, humandisulfidptosisendoplasmic reticulum stressglucose deprivationSLC7A11tumor

Identifiers

PMID39739602
PMCPMC11831432

What Socratic 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 Socratic graph.