Transcription factor CASZ1 increases an oncogenic transcriptional process in tumorigenesis and progression of glioma cells

Mao, Chaofu; Huang, Chengying; Hu, Zhicheng; Qu, Shanqiang

doi:10.1002/mco2.182

Cited by 14 publications

(16 citation statements)

References 31 publications

(52 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Maximum safe surgical resection combined with postoperative radiotherapy and chemotherapy is currently the mainstay of treatment for malignant gliomas ( 3 ). Despite advances in diagnosing and treating gliomas, there has been little impact on the outcomes of patients with malignant gliomas ( 4 , 5 ). Recent studies have found that tumor immune response plays an increasingly crucial role in the development of glioma ( 6 – 9 ), suggesting that immunotherapy holds great promise in treating glioma.…”

Section: Introductionmentioning

confidence: 99%

Classification related to immunogenic cell death predicts prognosis, immune microenvironment characteristics, and response to immunotherapy in lower-grade gliomas

et al. 2023

View full text Add to dashboard Cite

BackgroundImmunogenic cell death (ICD) is a form of cell death that elicits immune responses against the antigens found in dead or dying tumor cells. Growing evidence implies that ICD plays a significant role in triggering antitumor immunity. The prognosis for glioma remains poor despite many biomarkers being reported, and identifying ICD-related biomarkers is imminent for better-personalized management in patients with lower-grade glioma (LGG).Materials and methodsWe identified ICD-related differentially expressed genes (DEGs) by comparing gene expression profiles obtained across Genotype-Tissue Expression (GTEx) and The Cancer Genome Atlas (TCGA) cohorts. On the foundation of ICD-related DEGs, two ICD-related clusters were identified through consensus clustering. Then, survival analysis, functional enrichment analysis, somatic mutation analysis, and immune characteristics analysis were performed in the two ICD-related subtypes. Additionally, we developed and validated a risk assessment signature for LGG patients. Finally, we selected one gene (EIF2AK3) from the above risk model for experimental validation.Results32 ICD-related DEGs were screened, dividing the LGG samples from the TCGA database into two distinct subtypes. The ICD-high subgroup showed worse overall survival (OS), greater immune infiltration, more active immune response process, and higher expression levels of HLA genes than the ICD-low subgroup. Additionally, nine ICD-related DEGs were identified to build the prognostic signature, which was highly correlated with the tumor-immune microenvironment and could unambiguously be taken as an independent prognostic factor and further verified in an external dataset. The experimental results indicated that EIF2AK3 expression was higher in tumors than paracancerous tissues, and high-expression EIF2AK3 was enriched in WHO III and IV gliomas by qPCR and IHC, and Knockdown of EIF2AK3 suppressed cell viability and mobility in glioma cells.ConclusionWe established novel ICD-related subtypes and risk signature for LGG, which may be beneficial to improving clinical outcome prediction and guiding individualized immunotherapy.

show abstract

Section: Introductionmentioning

confidence: 99%

Classification related to immunogenic cell death predicts prognosis, immune microenvironment characteristics, and response to immunotherapy in lower-grade gliomas

et al. 2023

View full text Add to dashboard Cite

show abstract

“…Subsequently, this study investigated the TF activity within each disulfidoptosis-related subpopulation. Understanding TFs is crucial for deciphering gene regulatory networks, cellular development, and tumor occurrences ( 77 ). Single-cell level analysis in KIRC revealed distinct TF characteristics among fibroblasts, macrophages, monocytes, B cells, and T cell subtypes.…”

Section: Discussionmentioning

confidence: 99%

Single-cell disulfidptosis regulator patterns guide intercellular communication of tumor microenvironment that contribute to kidney renal clear cell carcinoma progression and immunotherapy

Xu,

Li,

Qian

et al. 2024

Front. Immunol.

View full text Add to dashboard Cite

BackgroundDisulfidptosis, an emerging type of programmed cell death, plays a pivotal role in various cancer types, notably impacting the progression of kidney renal clear cell carcinoma (KIRC) through the tumor microenvironment (TME). However, the specific involvement of disulfidptosis within the TME remains elusive.MethodsAnalyzing 41,784 single cells obtained from seven samples of KIRC through single-cell RNA sequencing (scRNA-seq), this study employed nonnegative matrix factorization (NMF) to assess 24 disulfidptosis regulators. Pseudotime analysis, intercellular communication mapping, determination of transcription factor activities (TFs), and metabolic profiling of the TME subgroup in KIRC were conducted using Monocle, CellChat, SCENIC, and scMetabolism. Additionally, public cohorts were utilized to predict prognosis and immune responses within the TME subgroup of KIRC.ResultsThrough NMF clustering and differential expression marker genes, fibroblasts, macrophages, monocytes, T cells, and B cells were categorized into four to six distinct subgroups. Furthermore, this investigation revealed the correlation between disulfidptosis regulatory factors and the biological traits, as well as the pseudotime trajectories of TME subgroups. Notably, disulfidptosis-mediated TME subgroups (DSTN+CD4T-C1 and FLNA+CD4T-C2) demonstrated significant prognostic value and immune responses in patients with KIRC. Multiple immunohistochemistry (mIHC) assays identified marker expression within both cell clusters. Moreover, CellChat analysis unveiled diverse and extensive interactions between disulfidptosis-mediated TME subgroups and tumor epithelial cells, highlighting the TNFSF12-TNFRSF12A ligand-receptor pair as mediators between DSTN+CD4T-C1, FLNA+CD4T-C2, and epithelial cells.ConclusionOur study sheds light on the role of disulfidptosis-mediated intercellular communication in regulating the biological characteristics of the TME. These findings offer valuable insights for patients with KIRC, potentially guiding personalized immunotherapy approaches.

show abstract

“…We were not able to validate TMPRSS2 fusions with CASZ1 , SIM2 , and C1orf61 due to the insufficient amount of RNA; however, all these genes are known to play roles in pathologic conditions, including cancers. CASZ1 encodes a zinc finger transcription factor whose dysregulated expression was linked to the pathobiology of neuroblastoma [ 46 ], glioma [ 47 ], and hepatocellular carcinoma, and aberrant fusion transcripts of CASZ1 were reported in colorectal and bladder cancers [ 48 ]. To date, no reports are linking CASZ1 to PCa.…”

Section: Discussionmentioning

confidence: 99%

Fusion sequencing via terminator‐assisted synthesis (FTAS‐seq) identifies TMPRSS2 fusion partners in prostate cancer

et al. 2023

View full text Add to dashboard Cite

Genetic rearrangements that fuse an androgen‐regulated promoter area with a protein‐coding portion of an originally androgen‐unaffected gene are frequent in prostate cancer, with the fusion between transmembrane serine protease 2 (TMPRSS2) and ETS transcription factor ERG (ERG) (TMPRSS2‐ERG fusion) being the most prevalent. Conventional hybridization‐ or amplification‐based methods can test for the presence of expected gene fusions, but the exploratory analysis of currently unknown fusion partners is often cost‐prohibitive. Here, we developed an innovative next‐generation sequencing (NGS)‐based approach for gene fusion analysis termed fusion sequencing via terminator‐assisted synthesis (FTAS‐seq). FTAS‐seq can be used to enrich the gene of interest while simultaneously profiling the whole spectrum of its 3′‐terminal fusion partners. Using this novel semi‐targeted RNA‐sequencing technique, we were able to identify 11 previously uncharacterized TMPRSS2 fusion partners and capture a range of TMPRSS2‐ERG isoforms. We tested the performance of FTAS‐seq with well‐characterized prostate cancer cell lines and utilized the technique for the analysis of patient RNA samples. FTAS‐seq chemistry combined with appropriate primer panels holds great potential as a tool for biomarker discovery that can support the development of personalized cancer therapies.

show abstract

Transcription factor CASZ1 increases an oncogenic transcriptional process in tumorigenesis and progression of glioma cells

Cited by 14 publications

References 31 publications

Classification related to immunogenic cell death predicts prognosis, immune microenvironment characteristics, and response to immunotherapy in lower-grade gliomas

Classification related to immunogenic cell death predicts prognosis, immune microenvironment characteristics, and response to immunotherapy in lower-grade gliomas

Single-cell disulfidptosis regulator patterns guide intercellular communication of tumor microenvironment that contribute to kidney renal clear cell carcinoma progression and immunotherapy

Fusion sequencing via terminator‐assisted synthesis (FTAS‐seq) identifies TMPRSS2 fusion partners in prostate cancer

Contact Info

Product

Resources

About