Based on disulfidptosis, revealing the prognostic and immunological characteristics of renal cell carcinoma with tumor thrombus of vena cava and identifying potential therapeutic target AJAP1

Yang, Lin; Li, Sheng; Liu, Xiaoqiang; Zheng, Fu-Chun; Xu, Songhui; Fu, Bin; Xiong, Jing

doi:10.1007/s00432-023-04877-x

Cited by 24 publications

(23 citation statements)

References 37 publications

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“…The proposed theory of disul dptosis provides a novel theoretical rationale for developing induced disul dptotic therapeutics against HCC [11]. Although disul dptosis has been observed in different types of tumors such as bladder cancer [18,19], renal cell carcinoma [20], thyroid carcinoma [21], there is still a considerable lack of understanding in relation to HCC. Our study demonstrated that the DRGs were markedly increased in HCC, indicating a strong correlation with an unfavorable prognosis, thus providing clari cation on the role of the disul dptosis process in HCC.…”

Section: Discussionmentioning

confidence: 99%

Personalized Therapies in Hepatocellular Carcinoma: Insights from a Disulfidptosis-Related Signature

Wan,

Xu,

Zhou

et al. 2024

Preprint

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Hepatocellular carcinoma (HCC) is the predominant pathological type of liver cancer with an unfavorable prognosis. Disulfidptosis is the newest cell death form and plays a vital role in tumorigenesis. However, the role of disulfidptosis-related genes (DRGs) in HCC remains unknown. The RNA-seq and clinical data of HCC patients were obtained from The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) databases. Based on DRGs in TCGA cohort, the predictive model was established via regression analysis of the least absolute shrinkage and selection operator (LASSO) and subsequently validated using ICGC cohort. Moreover, we investigated the relationship between predictive model and clinical features, somatic mutations, molecular mechanism, immune microenvironment and drug response. This study created an eight-gene signature. Here, we noticed a higher level of those eight genes in HCC patients in both RNA and protein levels. The patients in the high-risk group had a poor prognosis. It was found the predictive model was an independent prognostic factor by Multivariate Cox analyses. Pathways involved in cancer, cell membrane, and metabolism was significantly enriched. In addition, tumor mutation burden (TMB) and immune checkpoint genes expression were higher in the high-risk group. Furthermore, the high-risk group was more sensitive to immunotherapy and some targeted therapy. We comprehensively and systematically identified a new disulfidptosis-related signature, which could serve as a valuable tool for predicting prognosis, immune cell infiltration and therapy response of HCC patients. Thus, these discoveries could have potentially clinical value in directing personalized therapies in the future.

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Section: Discussionmentioning

confidence: 99%

Personalized Therapies in Hepatocellular Carcinoma: Insights from a Disulfidptosis-Related Signature

Wan,

Xu,

Zhou

et al. 2024

Preprint

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“…Additionally, the DRGs (FLNA, TLN1, PRDX1, MYH9, FLNB, ACTB, SLC7A11, RPN1, NCKAP1, NUBPL, NDUFA11, LRPPRC, OXSM, NDUFS1, and GYS1) were obtained from previous literature. 21,22 Detailed information about these genes is provided in Supporting Information: Table S1.…”

Section: Data Sourcesmentioning

confidence: 99%

Analysis of network expression and immune infiltration of disulfidptosis‐related genes in chronic obstructive pulmonary disease

Liu,

Zhu,

Wang

et al. 2024

Immunity Inflam & Disease

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BackgroundChronic obstructive pulmonary disease (COPD) is a globally prevalent respiratory disease, and programmed cell death plays a pivotal role in the development of COPD. Disulfidptosis is a newly discovered type of cell death that may be associated with the progression of COPD. However, the expression and role of disulfidptosis‐related genes (DRGs) in COPD remain unclear.MethodsThe expression of DRGs was identified by analyzing RNA sequencing (RNA‐seq) data in COPD. Further, COPD patients were classified into two subtypes by unsupervised cluster analysis to reveal their differences in gene expression and immune infiltration. Meanwhile, hub genes associated with disulfidptosis were screened by weighted gene co‐expression network analysis. Subsequently, the hub genes were validated experimentally in cells and animals. In addition, we screened potential therapeutic drugs through the hub genes.ResultsWe identified two distinct molecular clusters and observed significant differences in immune cell populations between them. In addition, we screened nine hub genes, and experimental validation showed that CDC71, DOHH, PDAP1, and SLC25A39 were significantly upregulated in cigarette smoke‐induced COPD mouse lung tissues and bronchial epithelial cells (BEAS‐2B) treated with cigarette smoke extract. Finally, we predicted 10 potential small molecule drugs such as Atovaquone, Taurocholic acid, Latamoxef, and Methotrexate.ConclusionWe highlighted the strong association between COPD and disulfidptosis, with DRGs demonstrating a discriminative capacity for COPD. Additionally, the expression of certain novel genes, including CDC71, DOHH, PDAP1, and SLC25A39, is linked to COPD and may aid in the diagnosis and assessment of this condition.

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“…Recent research has revealed a decrease in the expression of the disulfidptosis-related differential gene AJAP1 in clear cell renal cell carcinoma (ccRCC) tissues. This reduction establishes AJAP1 as a novel biomarker for ccRCC and suggests that it may be useful as a therapeutic target for ccRCC patients [ 29 ]. Peng and colleagues identified a link between ISG20 and disulfidptosis, as well as tumor immunity, indicating its potential as a therapeutic target for ccRCC [ 30 ].…”

Section: Disulfidptosis and Diseasementioning

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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Based on disulfidptosis, revealing the prognostic and immunological characteristics of renal cell carcinoma with tumor thrombus of vena cava and identifying potential therapeutic target AJAP1

Cited by 24 publications

References 37 publications

Personalized Therapies in Hepatocellular Carcinoma: Insights from a Disulfidptosis-Related Signature

Personalized Therapies in Hepatocellular Carcinoma: Insights from a Disulfidptosis-Related Signature

Analysis of network expression and immune infiltration of disulfidptosis‐related genes in chronic obstructive pulmonary disease

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

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