Disulfidptosis: a new form of programmed cell death

Zheng, Tingjin; Liu, Qingbo; Xing, Feiyue; Zeng, Chong; Wang, Weidong

doi:10.1186/s13046-023-02712-2

Cited by 73 publications

(65 citation statements)

References 13 publications

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“…Disulfidptosis is a novel form of PCD that is distinct compared with pyroptosis, ferroptosis and cuproptosis. There may be three indicators that disulfidptosis has been activated: (a) high expression of SLC7A11; (b) glucose deprivation conditions; and (c) formation of aberrant disulfide bonds 21 . Disulfidptosis has been recently explored in bladder cancer, hepatocellular carcinoma, lung adenocarcinoma, breast cancer, cervical cancer, colorectal cancer and thyroid carcinoma.…”

Section: Discussionmentioning

confidence: 99%

Disulfidptosis‐related PABPC3 promotes tumor progression and inhibits immune activity in osteosarcoma

Cao,

Wu,

et al. 2023

The Journal of Gene Medicine

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BackgroundOsteosarcoma is a very aggressive bone tumor mainly affecting teens and young adults. Disulfidptosis is a metabolic‐related form of regulated cell death. However, the interconnection between disulfidptosis and osteosarcoma has not been explored.MethodsIn the present study, disulfidptosis‐related clusters were identified in osteosarcoma using the nonnegative matrix factorization clustering method. PABPC3 was identified as a hazardous gene in osteosarcoma using machine learning algorithms, CoxBoost, and Random Survival Forest. The prognostic value, pathway annotation, immune characteristics, and drug prediction of PABPC3 were systematically explored. MTT (i.e., 3‐(4, 5‐dimethyl thiazol‐2‐yl)‐2,5‐diphenytetrazolium bromide), EdU (ie. 5‐ethyny‐2'‐deoxvuridine), and Transwell assays were used for in vitro validation of PABPC3.ResultsThe disulfidptosis‐related clusters could distinguish survival outcomes of osteosarcoma patients. PABPC3 could predict survival outcomes, immune activity, and drug response in osteosarcoma patients. Besides, PABPC3 was proven to facilitate the proliferation and migration of osteosarcoma.ConclusionsThe present study is expected to establish the bridge between disulfidptosis and osteosarcoma. PABPC3 is expected to be further explored as a therapeutic target in osteosarcoma.

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Section: Discussionmentioning

confidence: 99%

Disulfidptosis‐related PABPC3 promotes tumor progression and inhibits immune activity in osteosarcoma

Cao,

Wu,

et al. 2023

The Journal of Gene Medicine

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“…Since the optimal sequencing of drug therapy for patients with hepatocellular carcinoma has not yet been determined, there is an urgent need for predictive biomarkers to inform the choice of hepatocellular therapy [13] . Disu dptosis is a newly discovered form of cell death, as disu dptosis-related genes are a new form of cell death triggered by disul de stress, which is mainly characterized by the progressive accumulation of intracellular disul de leading to the collapse of cytoskeletal proteins and Factin, and this discovery helps to develop new therapeutic strategies for LIHC against cancer [14] .In disu dptosis, disul de is a relatively stable product that acts mainly by acting as an inter-and intrasubunit cross-link, thus maintaining the spatial structure of the protein including secondary, tertiary and quaternary structures, which confer physical and chemical stability to the protein. Since disul des are produced in response to stress, it is important to better understand how disul de accumulation leads to cell death.…”

Section: Discussionmentioning

confidence: 99%

Disulfidptosis-related lncRNAs predict prognosis and immune response of Liver hepatocellular carcinoma

Li,

Xing,

Luo

et al. 2023

Preprint

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Background Liver hepatocellular carcinoma(LIHC) is the most common types of cancers.LncRNA has a very important role in the disease progression of LIHC, meanwhile, disufidptosis is a newly discovered mode of tumor cell death that has received high attention.Therefore, we explored the relationship of disufidptosis-related lncRNAs(DTLNS) with clinical prognosis, immunotherapy and drug sensitivity in the LIHC. Methods RNA-expression profiling and clinical data were obtained from The Cancer Genome Atlas (TCGA), and 10 disufidptosis-related genes were obtained from the correlation Studies.The prognostic characteristics were constructed by co-expression analysis, lasso regression and Cox regression analysis. Patients were divided into high and low risk groups. Subsequently, gene ontology (GO), Kyoto Encyclopedia of Gene and Genome Enrichment (KEGG), immune-related function and tumor mutational load (TMB) analyses were performed by the DTLNS. Finally, we used the Tumor Immune Dysfunction and Exclusion (TIDE) algorithm to predict the immune escape and immunotherapy by the DTLNS, -and to determine the sensitivity to potential LIHC drugs. Results A totle of 424 DTLNS were obtained, and a prognostic signature was developed. We found that high-risk patients had worse overall survival (OS) and progression-free survival (PFS) and mortality. Independent prognostic analyses, ROC, C-index and nomogram showed that the DTLNS can accurately predict the prognosis of patients. KEGG enrichment analysis showed that the biological functions of DTLNS patients. We found that immune-related functions were suppressed in LIHC patients with disufidptosis-related genes mutations. Conclusion To conclude,the 424 DTLNS can effectively predict the prognosis of LIHC patients and may provide new insights into clinical applications and immunotherapy.

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“…However, recent research has provided a different perspective. It suggests that when glucose levels are low, increased expression of SLC7A11 paradoxically accelerates cell death [ 8 – 13 , 50 – 52 ]. For example, in glioblastoma cells starved for glucose, cystine uptake via xCT (with SLC7A11 as the catalytic subunit) leads to NADPH depletion, ROS accumulation, and cell death [ 50 ].…”

Section: Historical Overview Of Disulfidptosis Discoverymentioning

confidence: 99%

“…This assembly may exacerbate the formation of disulfide bonds within F-actin. It accomplishes this by promoting Arp2/3-mediated lamellipodia formation, which is a critical step in disulfidptosis [ 8 , 10 – 13 ].…”

Section: Introductionmentioning

confidence: 99%

Disulfidptosis decoded: a journey through cell death mysteries, regulatory networks, disease paradigms and future directions

Chen,

Ma,

Yang

et al. 2024

Biomark Res

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Cell death is an important part of the life cycle, serving as a foundation for both the orderly development and the maintenance of physiological equilibrium within organisms. This process is fundamental, as it eliminates senescent, impaired, or aberrant cells while also promoting tissue regeneration and immunological responses. A novel paradigm of programmed cell death, known as disulfidptosis, has recently emerged in the scientific circle. Disulfidptosis is defined as the accumulation of cystine by cancer cells with high expression of the solute carrier family 7 member 11 (SLC7A11) during glucose starvation. This accumulation causes extensive disulfide linkages between F-actins, resulting in their contraction and subsequent detachment from the cellular membrane, triggering cellular death. The RAC1-WRC axis is involved in this phenomenon. Disulfidptosis sparked growing interest due to its potential applications in a variety of pathologies, particularly oncology, neurodegenerative disorders, and metabolic anomalies. Nonetheless, the complexities of its regulatory pathways remain elusive, and its precise molecular targets have yet to be definitively identified. This manuscript aims to meticulously dissect the historical evolution, molecular underpinnings, regulatory frameworks, and potential implications of disulfidptosis in various disease contexts, illuminating its promise as a groundbreaking therapeutic pathway and target.

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Disulfidptosis: a new form of programmed cell death

Abstract: Disulfidptosis, a new form of cell death triggered by disulfide stress, is characterized by the collapse of cytoskeleton proteins and F-actin due to the intracellular accumulation of disulfides. This discovery will eventually aid in the development of therapeutic strategies against cancer.

Cited by 73 publications

References 13 publications

Disulfidptosis‐related PABPC3 promotes tumor progression and inhibits immune activity in osteosarcoma

Disulfidptosis‐related PABPC3 promotes tumor progression and inhibits immune activity in osteosarcoma

Disulfidptosis-related lncRNAs predict prognosis and immune response of Liver hepatocellular carcinoma

Disulfidptosis decoded: a journey through cell death mysteries, regulatory networks, disease paradigms and future directions

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