Prognostic Prediction Model for Glioblastoma: A Ferroptosis-Related Gene Prediction Model and Independent External Validation

Chen, Wenlin; Lei, Chuxiang; Wang, Yuekun; Guo, Dan; Wang, Xiaoxi; Zhang, Zixin; Wang, Yu; Ma, Wenbin

doi:10.3390/jcm12041341

Cited by 6 publications

(4 citation statements)

References 40 publications

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“…As a newly discovered type of cell death, ferroptosis has been proposed as an attractive target in GBM [109]. In support of this, ferroptosis-related genes have recently been indicated with a prognostic value for GBM [110]. Moreover, the SERBP inhibitor fatostatin has been shown to trigger ferroptosis in GBM cell lines by hindering GPX4 synthesis [111].…”

Section: Ferroptosismentioning

confidence: 96%

Emerging Lipid Targets in Glioblastoma

Darwish,

Pammer,

Gallyas

et al. 2024

Cancers

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GBM accounts for most of the fatal brain cancer cases, making it one of the deadliest tumor types. GBM is characterized by severe progression and poor prognosis with a short survival upon conventional chemo- and radiotherapy. In order to improve therapeutic efficiency, considerable efforts have been made to target various features of GBM. One of the targetable features of GBM is the rewired lipid metabolism that contributes to the tumor’s aggressive growth and penetration into the surrounding brain tissue. Lipid reprogramming allows GBM to acquire survival, proliferation, and invasion benefits as well as supportive modulation of the tumor microenvironment. Several attempts have been made to find novel therapeutic approaches by exploiting the lipid metabolic reprogramming in GBM. In recent studies, various components of de novo lipogenesis, fatty acid oxidation, lipid uptake, and prostaglandin synthesis have been considered promising targets in GBM. Emerging data also suggest a significant role hence therapeutic potential of the endocannabinoid metabolic pathway in GBM. Here we review the lipid-related GBM characteristics in detail and highlight specific targets with their potential therapeutic use in novel antitumor approaches.

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Section: Ferroptosismentioning

confidence: 96%

Emerging Lipid Targets in Glioblastoma

Darwish,

Pammer,

Gallyas

et al. 2024

Cancers

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“…In evaluating patients with primary breast cancer, including ChaC1 mRNA expression levels in the scoring model led to changes in chemotherapy decisions in 16% of patients ( 152 ). In addition, ChaC1 has been included in prognostic models of renal cell carcinoma ( 153 ) and glioblastoma ( 154 ). Including ChaC1 in tumor prognosis predictions may guide personalized treatment options.…”

Section: Role Of Gsh-degrading Enzymes In Medicinementioning

confidence: 99%

Glutathione‑degrading enzymes in the complex landscape of tumors (Review)

Zhang,

Yao2,

Zhou

et al. 2024

Int J Oncol

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Glutathione (GSH)-degrading enzymes are essential for starting the first stages of GSH degradation. These enzymes include extracellular γ-glutamyl transpeptidase (GGT) and intracellular GSH-specific γ-glutamylcyclotransferase 1 (ChaC1) and 2. These enzymes are essential for cellular activities, such as immune response, differentiation, proliferation, homeostasis regulation and programmed cell death. Tumor tissue frequently exhibits abnormal expression of GSH-degrading enzymes, which has a key impact on the development and spread of malignancies. The present review summarizes gene and protein structure, catalytic activity and regulation of GSH-degrading enzymes, their vital roles in tumor development (including regulation of oxidative and endoplasmic reticulum stress, control of programmed cell death, promotion of inflammation and tumorigenesis and modulation of drug resistance in tumor cells) and potential role as diagnostic biomarkers and therapeutic targets. Contents 1. Introduction 2. Extracellular and intracellular GSH-degrading enzymes 3. GSH-degrading enzymes in tumorigenesis and progression 4. Role of GSH-degrading enzymes in medicine 5. Conclusion

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“…Glioblastoma is a highly invasive malignant brain tumor, characterized by significant biological heterogeneity and varying treatment responses. Abnormal expression of the CRYAB gene has become a focus in studying the mechanisms underlying glioblastoma development ( 21 ). In the realm of cellular stress response, CRYAB, an integral member of the heat shock protein (HSP) family, actively engages in cellular stress responses, affording protection to cells against the deleterious effects provoked by environmental stressors and cellular stressors.…”

Section: Introductionmentioning

confidence: 99%

Single cell sequencing revealed the mechanism of CRYAB in glioma and its diagnostic and prognostic value

Cai,

Zhao,

et al. 2024

Front. Immunol.

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BackgroundWe explored the characteristics of single-cell differentiation data in glioblastoma and established prognostic markers based on CRYAB to predict the prognosis of glioblastoma patients. Aberrant expression of CRYAB is associated with invasive behavior in various tumors, including glioblastoma. However, the specific role and mechanisms of CRYAB in glioblastoma are still unclear.MethodsWe assessed RNA-seq and microarray data from TCGA and GEO databases, combined with scRNA-seq data on glioma patients from GEO. Utilizing the Seurat R package, we identified distinct survival-related gene clusters in the scRNA-seq data. Prognostic pivotal genes were discovered through single-factor Cox analysis, and a prognostic model was established using LASSO and stepwise regression algorithms. Moreover, we investigated the predictive potential of these genes in the immune microenvironment and their applicability in immunotherapy. Finally, in vitro experiments confirmed the functional significance of the high-risk gene CRYAB.ResultsBy analyzing the ScRNA-seq data, we identified 28 cell clusters representing seven cell types. After dimensionality reduction and clustering analysis, we obtained four subpopulations within the oligodendrocyte lineage based on their differentiation trajectory. Using CRYAB as a marker gene for the terminal-stage subpopulation, we found that its expression was associated with poor prognosis. In vitro experiments demonstrated that knocking out CRYAB in U87 and LN229 cells reduced cell viability, proliferation, and invasiveness.ConclusionThe risk model based on CRYAB holds promise in accurately predicting glioblastoma. A comprehensive study of the specific mechanisms of CRYAB in glioblastoma would contribute to understanding its response to immunotherapy. Targeting the CRYAB gene may be beneficial for glioblastoma patients.

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Prognostic Prediction Model for Glioblastoma: A Ferroptosis-Related Gene Prediction Model and Independent External Validation

Cited by 6 publications

References 40 publications

Emerging Lipid Targets in Glioblastoma

Emerging Lipid Targets in Glioblastoma

Glutathione‑degrading enzymes in the complex landscape of tumors (Review)

Single cell sequencing revealed the mechanism of CRYAB in glioma and its diagnostic and prognostic value

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