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  • Tan, Guowei  (5)
  • Zhao, Wenpeng  (5)
  • 1
    Online Resource
    Online Resource
    The CDK inhibitor AT7519 inhibits human glioblastoma cell growth by inducing apoptosis, pyroptosis and cell cycle arrest
    Springer Science and Business Media LLC ; 2023
    In:  Cell Death & Disease Vol. 14, No. 1 ( 2023-01-09)
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    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 14, No. 1 ( 2023-01-09)
    Abstract: Glioblastoma multiforme (GBM) is the most lethal primary brain tumor with a poor median survival of less than 15 months. However, clinical strategies and effective therapies are limited. Here, we found that the second-generation small molecule multi-CDK inhibitor AT7519 is a potential drug for GBM treatment according to high-throughput screening via the Approved Drug Library and Clinical Compound Library (2718 compounds). We found that AT7519 significantly inhibited the cell viability and proliferation of U87MG, U251, and patient-derived primary GBM cells in a dose-dependent manner. Furthermore, AT7519 also inhibited the phosphorylation of CDK1/2 and arrested the cell cycle at the G1-S and G2-M phases. More importantly, AT7519 induced intrinsic apoptosis and pyroptosis via caspase-3-mediated cleavage of gasdermin E (GSDME). In the glioblastoma intracranial and subcutaneous xenograft assays, tumor volume was significantly reduced after treatment with AT7519. In summary, AT7519 induces cell death through multiple pathways and inhibits glioblastoma growth, indicating that AT7519 is a potential chemical available for GBM treatment.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    URL: Article
    DOI: 10.1038/s41419-022-05528-8
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2541626-1
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  • 2
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    Online Resource
    Association between chronic periodontitis and the risk of Alzheimer’s disease: combination of text mining and GEO dataset
    Springer Science and Business Media LLC ; 2021
    In:  BMC Oral Health Vol. 21, No. 1 ( 2021-09-23)
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    In: BMC Oral Health, Springer Science and Business Media LLC, Vol. 21, No. 1 ( 2021-09-23)
    Abstract: Although chronic periodontitis has previously been reported to be linked with Alzheimer's disease (AD), the pathogenesis between the two is unclear. The purpose of this study is to analyze and screen the relevant and promising molecular markers between chronic periodontitis and Alzheimer's disease (AD). Methods In this paper, we analyzed three AD expression datasets and extracted differentially expressed genes (DEGs), then intersected them with chronic periodontitis genes obtained from text mining, and finally obtained integrated DEGs. We followed that by enriching the matching the matching cell signal cascade through DAVID analysis. Moreover, the MCODE of Cytoscape software was employed to uncover the protein–protein interaction (PPI) network and the matching hub gene. Finally, we verified our data using a different independent AD cohort. Results The chronic periodontitis gene set acquired from text abstracting was intersected with the previously obtained three AD groups, and 12 common genes were obtained. Functional enrichment assessment uncovered 12 cross-genes, which were mainly linked to cell morphogenesis involved in neuron differentiation, leading edge membrane, and receptor ligand activity. After PPI network creation, the ten hub genes linked to AD were retrieved, consisting of SPP1, THY1, CD44, ITGB1, HSPB3, CREB1, SST, UCHL1, CCL5 and BMP7. Finally, the function terms in the new independent dataset were used to verify the previous dataset, and we found 22 GO terms and one pathway, "ECM-receptor interaction pathways", in the overlapping functional terms. Conclusions The establishment of the above-mentioned candidate key genes, as well as the enriched signaling cascades, provides promising molecular markers for chronic periodontitis-related AD, which may help the diagnosis and treatment of AD patients in the future.
    Type of Medium: Online Resource
    ISSN: 1472-6831
    URL: Article
    DOI: 10.1186/s12903-021-01827-2
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2091511-1
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  • 3
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    New Autophagy-Ferroptosis Gene Signature Predicts Survival in Glioma
    Frontiers Media SA ; 2021
    In:  Frontiers in Cell and Developmental Biology Vol. 9 ( 2021-11-15)
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    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 9 ( 2021-11-15)
    Abstract: Background: Ferroptosis plays an important role in glioma and significantly affects the prognosis, but the specific mechanism has not yet been elucidated. Recent studies suggest that autophagy regulates the process of ferroptosis. This study aimed to find potential autophagy-ferroptosis genes and explore the prognostic significance in glioma. Methods: Ferroptosis and autophagy genes were obtained from two online databases (zhounan.org/ferrdb and autophagy.lu/). The RNAseq data and clinical information were obtained from the Chinese Glioma Genome Atlas (CGGA) database ( http://www.cgga.org.cn/ ). Univariate, multivariate, lasso and Cox regression analysis screened out prognosis-related genes, and a risk model was constructed. Receiver operating characteristic (ROC) curve analysis evaluated the predictive efficiency of the model. Finally, a nomogram was constructed to more accurately predict the prognosis of glioma. Results: We developed a Venn diagram showing 23 autophagy-ferroptosis genes. A total of 660 cases (including RNA sequences and complete clinical information) from two different cohorts (training group n = 413, verification group n = 247) of the CGGA database was acquired. Cohorts were screened to include five prognosis-related genes ( MTOR , BID , HSPA5 , CDKN2A , GABARAPLA2 ). Kaplan-Meier curves showed that the risk model was a good prognostic indicator ( p & lt; 0.001). ROC analysis showed good efficacy of the risk model. Multivariate Cox analysis also revealed that the risk model was suitable for clinical factors related to prognosis, including type of disease (primary, recurrence), grade (III-IV), age, temozolomide treatment, and 1p19q state. Using the five prognosis-related genes and the risk score, we constructed a nomogram assessed by C-index (0.7205) and a calibration plot that could more accurately predict glioma prognosis. Conclusion: Using a current database of autophagy and ferroptosis genes, we confirmed the prognostic significance of autophagy-ferroptosis genes in glioma, and we constructed a prognostic model to help guide treatment for high grade glioma in the future.
    Type of Medium: Online Resource
    ISSN: 2296-634X
    URL: Article
    DOI: 10.3389/fcell.2021.739097
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2737824-X
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  • 4
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    Identification of ubiquitin-specific protease 32 as an oncogene in glioblastoma and the underlying mechanisms
    Springer Science and Business Media LLC ; 2022
    In:  Scientific Reports Vol. 12, No. 1 ( 2022-04-19)
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    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 12, No. 1 ( 2022-04-19)
    Abstract: Glioblastoma (GBM) patients present poor prognosis. Deubiquitination by deubiquitinating enzymes (DUBs) is a critical process in cancer progression. Ubiquitin-specific proteases (USPs) constitute the largest sub-family of DUBs. Evaluate the role of USP32 in GBM progression and provide a potential target for GBM treatment. Clinical significance of USP32 was investigated using Gene Expression Omnibus databases. Effects of USP32 on cell growth and metastasis were studied in vitro and in vivo. Differentially expressive genes between USP32-knockdown U-87 MG cells and negative control cells were detected using RNA sequencing and used for Gene Ontology and Kyoto Encyclopedia of Genes and Genomic pathway enrichment analyses. Finally, RT-qPCR was used to validate the divergent expression of genes involved in the enriched pathways. USP32 was upregulated in GBM patients, being correlated to poor prognosis. USP32 downregulation inhibited cell growth and metastasis in vitro. Furthermore, USP32 knockdown inhibited tumorigenesis in vivo. In addition, UPS32 was identified as a crucial regulator in different pathways including cell cycle, cellular senescence, DNA replication, base excision repair, and mismatch repair pathways. USP32 acts as an oncogene in GBM through regulating several biological processes/pathways. It could be a potential target for GBM treatment.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-022-09497-y
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2615211-3
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  • 5
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    Online Resource
    Development of an Immune-Related Prognostic Index Associated With Glioblastoma
    Frontiers Media SA ; 2021
    In:  Frontiers in Neurology Vol. 12 ( 2021-5-19)
    Details
    In: Frontiers in Neurology, Frontiers Media SA, Vol. 12 ( 2021-5-19)
    Abstract: Background: Although the tumor microenvironment (TME) is known to influence the prognosis of glioblastoma (GBM), the underlying mechanisms are not clear. This study aims to identify hub genes in the TME that affect the prognosis of GBM. Methods: The transcriptome profiles of the central nervous systems of GBM patients were downloaded from The Cancer Genome Atlas (TCGA). The ESTIMATE scoring algorithm was used to calculate immune and stromal scores. The application of these scores in histology classification was tested. Univariate Cox regression analysis was conducted to identify genes with prognostic value. Subsequently, functional enrichment analysis and protein–protein interaction (PPI) network analysis were performed to reveal the pathways and biological functions associated with the genes. Next, these prognosis genes were validated in an independent GBM cohort from the Chinese Glioma Genome Atlas (CGGA). Finally, the efficacy of current antitumor drugs targeting these genes against glioma was evaluated. Results: Gene expression profiles and clinical data of 309 GBM samples were obtained from TCGA database. Higher immune and stromal scores were found to be significantly correlated with tissue type and poor overall survival (OS) ( p = 0.15 and 0.77, respectively). Functional enrichment analysis identified 860 upregulated and 162 downregulated cross genes, which were mainly linked to immune response, inflammatory response, cell membrane, and receptor activity. Survival analysis identified 228 differentially expressed genes associated with the prognosis of GBM ( p ≤ 0.05). A total of 48 hub genes were identified by the Cytoscape tool, and pathway enrichment analysis of the genes was performed using Database for Annotation, Visualization and Integrated Discovery (DAVID). The 228 genes were validated in an independent GBM cohort from the CGGA. In total, 10 genes were found to be significantly associated with prognosis of GBM. Finally, 14 antitumor drugs were identified by drug–gene interaction analysis. Conclusions: Here, 10 TME-related genes and 14 corresponding antitumor agents were found to be associated with the prognosis and OS of GBM.
    Type of Medium: Online Resource
    ISSN: 1664-2295
    URL: Article
    DOI: 10.3389/fneur.2021.610797
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2564214-5
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