Evidence map›Paper›PMID 38420162›Full record

ArticleMedComm2024

Multi-omics analysis of disulfidptosis regulators and therapeutic potential reveals glycogen synthase 1 as a disulfidptosis triggering target for triple-negative breast cancer.

Jindong Xie, Xinpei Deng, Yi Xie, Hongbo Zhu, Peng Liu, Wei Deng, Li Ning, Yuhui Tang, Yuying Sun, Hailin Tang and 3 more

Abstract read
In one paragraph

Article in MedComm, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing 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

58 citing papers in PubMed.

  1. Disulfidptosis: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026
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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

13 authors.

Jindong XieState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center for Cancer Sun Yat-Sen University Cancer Center Guangzhou Guangdong China.
Xinpei DengState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center for Cancer Sun Yat-Sen University Cancer Center Guangzhou Guangdong China.
Yi XieState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center for Cancer Sun Yat-Sen University Cancer Center Guangzhou Guangdong China.
Hongbo ZhuThe First Affiliated Hospital Hengyang Medical School University of South China Hengyang Hunan China.
Peng LiuState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center for Cancer Sun Yat-Sen University Cancer Center Guangzhou Guangdong China.
Wei DengState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center for Cancer Sun Yat-Sen University Cancer Center Guangzhou Guangdong China.
Li NingState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center for Cancer Sun Yat-Sen University Cancer Center Guangzhou Guangdong China.
Yuhui TangState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center for Cancer Sun Yat-Sen University Cancer Center Guangzhou Guangdong China.
Yuying SunState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center for Cancer Sun Yat-Sen University Cancer Center Guangzhou Guangdong China.
Hailin TangState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center for Cancer Sun Yat-Sen University Cancer Center Guangzhou Guangdong China.ORCID https://orcid.org/0000-0002-3206-782X
Manbo CaiThe First Affiliated Hospital Hengyang Medical School University of South China Hengyang Hunan China.
Xiaoming XieState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center for Cancer Sun Yat-Sen University Cancer Center Guangzhou Guangdong China.
Yutian ZouState Key Laboratory of Oncology in South China Guangdong Provincial Clinical Research Center for Cancer Sun Yat-Sen University Cancer Center Guangzhou Guangdong China.ORCID https://orcid.org/0000-0002-5205-9923

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disruption of disulfide homeostasis during biological processes can have fatal consequences. Excess disulfides induce cell death in a novel manner, termed as "disulfidptosis." However, the specific mechanism of disulfidptosis has not yet been elucidated. To determine the cancer types sensitive to disulfidptosis and outline the corresponding treatment strategies, we firstly investigated the crucial functions of disulfidptosis regulators pan-cancer at multi-omics levels. We found that different tumor types expressed dysregulated levels of disulfidptosis regulators, most of which had an impact on tumor prognosis. Moreover, we calculated the disulfidptosis activity score in tumors and validated it using multiple independent datasets. Additionally, we found that disulfidptosis activity was correlated with classic biological processes and pathways in various cancers. Disulfidptosis activity was also associated with tumor immune characteristics and could predict immunotherapy outcomes. Notably, the disulfidptosis regulator, glycogen synthase 1 (

Indexed as

disulfidptosispan‐cancerprognosissingle‐cell RNA‐seqtumor microenvironment

Identifiers

PMID38420162
PMCPMC10901283

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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.