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  • 1
    Online Resource
    Online Resource
    CRB2 enhances malignancy of glioblastoma via activation of the NF-κB pathway
    Elsevier BV ; 2022
    In:  Experimental Cell Research Vol. 414, No. 1 ( 2022-05), p. 113077-
    Details
    In: Experimental Cell Research, Elsevier BV, Vol. 414, No. 1 ( 2022-05), p. 113077-
    Type of Medium: Online Resource
    ISSN: 0014-4827
    URL: Article
    DOI: 10.1016/j.yexcr.2022.113077
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 1466780-0
    SSG: 12
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  • 2
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    FABP5 enhances malignancies of lower‐grade gliomas via canonical activation of NF‐κB signaling
    Wiley ; 2021
    In:  Journal of Cellular and Molecular Medicine Vol. 25, No. 9 ( 2021-05), p. 4487-4500
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 25, No. 9 ( 2021-05), p. 4487-4500
    Abstract: Low‐grade gliomas (LGGs) are grade III gliomas based on the WHO classification with significant genetic heterogeneity and clinical properties. Traditional histological classification of gliomas has been challenged by the improvement of molecular stratification; however, the reproducibility and diagnostic accuracy of LGGs classification still remain poor. Herein, we identified fatty acid binding protein 5 (FABP5) as one of the most enriched genes in malignant LGGs and elevated FABP5 revealed severe outcomes in LGGs. Functionally, lentiviral suppression of FABP5 reduced malignant characters including proliferation, cloning formation, immigration, invasion and TMZ resistance, contrarily, the malignancies of LGGs were enhanced by exogenous overexpression of FABP5. Mechanistically, epithelial‐mesenchymal transition (EMT) was correlated to FABP5 expression in LGGs and tumour necrosis factor α (TNFα)‐dependent NF‐κB signalling was involved in this process. Furthermore, FABP5 induced phosphorylation of inhibitor of nuclear factor kappa‐B kinase α (IKKα) thus activated nuclear factor kappa‐B (NF‐κB) signalling. Taken together, our study indicated that FABP5 enhances malignancies of LGGs through canonical activation of NF‐κB signalling, which could be used as individualized prognostic biomarker and potential therapeutic target of LGGs.
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.v25.9
    DOI: 10.1111/jcmm.16536
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2076114-4
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  • 3
    Online Resource
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    DataSheet_1.zip
    Frontiers Media SA ; 2022
    In:  Frontiers in Oncology Vol. 12 ( 2022-5-12)
    Details
    In: Frontiers in Oncology, Frontiers Media SA, Vol. 12 ( 2022-5-12)
    Abstract: Lower-grade gliomas (LGGs) are characterized by remarkable genetic heterogeneity and different clinical outcomes. Classification of LGGs is improved by the development of molecular stratification markers including IDH mutation and 1p/19q chromosomal integrity, which are used as a hallmark of survival and therapy sensitivity of LGG patients. However, the reproducibility and sensitivity of the current classification remain ambiguous. This study aimed to construct more accurate risk-stratification approaches. Methods According to bioinformatics, the sequencing profiles of methylation and transcription and imaging data derived from LGG patients were analyzed and developed predictable risk score and radiomics score. Moreover, the performance of predictable models was further validated. Results In this study, we determined a cluster of 6 genes that were correlated with IDH mutation/1p19q co-deletion status. Risk score model was calculated based on 6 genes and showed gratifying sensitivity and specificity for survival prediction and therapy response of LGG patients. Furthermore, a radiomics risk score model was established to noninvasively assist judgment of risk score in pre-surgery. Taken together, a predictable nomogram that combined transcriptional signatures and clinical characteristics was established and validated to be preferable to the histopathological classification. Our novel multi-omics nomograms showed a satisfying performance. To establish a user-friendly application, the nomogram was further developed into a web-based platform: https://drw576223193.shinyapps.io/Nomo/ , which could be used as a supporting method in addition to the current histopathological-based classification of gliomas. Conclusions Our novel multi-omics nomograms showed the satisfying performance of LGG patients and assisted clinicians to draw up individualized clinical management.
    Type of Medium: Online Resource
    ISSN: 2234-943X
    URL: Article
    URL: Article
    DOI: 10.3389/fonc.2022.729002
    DOI: 10.3389/fonc.2022.729002.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2649216-7
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  • 4
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    A Novel Risk Score Model Based on Eleven Extracellular Matrix-Related Genes for Predicting Overall Survival of Glioma Patients
    Hindawi Limited ; 2022
    In:  Journal of Oncology Vol. 2022 ( 2022-4-29), p. 1-20
    Details
    In: Journal of Oncology, Hindawi Limited, Vol. 2022 ( 2022-4-29), p. 1-20
    Abstract: Gliomas are the most common lethal primary brain tumors with variable survival outcomes for patients. The extracellular matrix (ECM) is linked with clinical prognosis of glioma patients, but it is not commonly used as a clinical indicator. Herein, we investigated changes in ECM-related genes (ECMRGs) via analyzing the transcriptional data of 938 gliomas from TCGA and CGGA datasets. Based on least absolute shrinkage and selection operator (LASSO) Cox regression analysis, a 11-ECMRG signature that is strongly linked with overall survival (OS) in glioma patients was identified. This signature was characterized by high-risk and low-risk score patterns. We found that the patients in the high-risk group are significantly linked with malignant molecular features and worse outcomes. Univariate and multivariate Cox regression analyses suggested that the signature is an independent indicator for glioma prognosis. The prediction accuracy of the signature was verified through time-dependent receiver operating characteristic (ROC) curves and calibration plots. Further bioinformatics analyses implied that the ECMRG signature is strongly associated with the activation of multiple oncogenic and metabolic pathways and immunosuppressive tumor microenvironment in gliomas. In addition, we confirmed that the high-risk score is an indicator for a therapy-resistant phenotype. In addition to bioinformatics analyses, we functionally verified the oncogenic role of bone morphogenetic protein 1 (BMP1) in gliomas in vitro.
    Type of Medium: Online Resource
    ISSN: 1687-8469 , 1687-8450
    URL: Article
    DOI: 10.1155/2022/4966820
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2461349-6
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  • 5
    Online Resource
    Online Resource
    NEK2 enhances malignancies of glioblastoma via NIK/NF-κB pathway
    Springer Science and Business Media LLC ; 2022
    In:  Cell Death & Disease Vol. 13, No. 1 ( 2022-01-14)
    Details
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 13, No. 1 ( 2022-01-14)
    Abstract: Glioblastoma (GBM) is one of the most lethal primary brain tumor with a poor median survival less than 15 months. Despite the development of the clinical strategies over the decades, the outcomes for GBM patients remain dismal due to the strong proliferation and invasion ability and the acquired resistance to radiotherapy and chemotherapy. Therefore, developing new biomarkers and therapeutic strategies targeting GBM is in urgent need. In this study, gene expression datasets and relevant clinical information were extracted from public cancers/glioma datasets, including TCGA, GRAVENDEEL, REMBRANDT, and GILL datasets. Differentially expressed genes were analyzed and NEK2 was picked as a candidate gene for subsequent validation. Human tissue samples and corresponding data were collected from our center and detected by immunohistochemistry analysis. Molecular biological assays and in vivo xenograft transplantation were performed to confirm the bioinformatic findings. High-throughput RNA sequencing, followed by KEGG analysis, GSEA analysis and GO analysis were conducted to identify potential signaling pathways related to NEK2 expression. Subsequent mechanism assays were used to verify the relationship between NEK2 and NF-κB signaling. Overall, we identified that NEK2 is significantly upregulated in GBM and the higher expression of NEK2 exhibited a poorer prognosis. Functionally, NEK2 knockdown attenuated cell proliferation, migration, invasion, and tumorigenesis of GBM while NEK2 overexpression promoted the GBM progression. Furthermore, High-throughput RNA sequencing and bioinformatics analysis indicated that NEK2 was positively related to the NF-κB signaling pathway in GBM. Mechanically, NEK2 activated the noncanonical NF-κB signaling pathway by phosphorylating NIK and increasing the activity and stability of NIK. In conclusion, NEK2 promoted the progression of GBM through activation of noncanonical NF-κB signaling, indicating that NEK2- NF-κB axis could be a potential drug target for GBM.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    URL: Article
    DOI: 10.1038/s41419-022-04512-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2541626-1
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  • 6
    Online Resource
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    Datasheet3.csv
    Frontiers Media SA ; 2023
    In:  Frontiers in Surgery Vol. 10 ( 2023-1-26)
    Details
    In: Frontiers in Surgery, Frontiers Media SA, Vol. 10 ( 2023-1-26)
    Abstract: Studies have shown that Nicotinamide adenine dinucleotide (NAD+) metabolism can promote the occurrence and development of glioma. However, the specific effects and mechanisms of NAD+ metabolism in glioma are unclear and there were no systematic researches about NAD+ metabolism related genes to predict the survival of patients with glioma. Methods The research was performed based on expression data of glioma cases in the Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) databases. Firstly, TCGA-glioma cases were classified into different subtypes based on 49 NAD+ metabolism-related genes (NMRGs) by consensus clustering. NAD+ metabolism-related differentially expressed genes (NMR-DEGs) were gotten by intersecting the 49 NMRGs and differentially expressed genes (DEGs) between normal and glioma samples. Then a risk model was built by Cox analysis and the least shrinkage and selection operator (LASSO) regression analysis. The validity of the model was verified by survival curves and receiver operating characteristic (ROC) curves. In addition, independent prognostic analysis of the risk model was performed by Cox analysis. Then, we also identified different immune cells, HLA family genes and immune checkpoints between high and low risk groups. Finally, the functions of model genes at single-cell level were also explored. Results Consensus clustering classified glioma patients into two subtypes, and the overall survival (OS) of the two subtypes differed. A total of 11 NAD+ metabolism-related differentially expressed genes (NMR-DEGs) were screened by overlapping 5,995 differentially expressed genes (DEGs) and 49 NAD+ metabolism-related genes (NMRGs). Next, four model genes, PARP9, BST1, NMNAT2, and CD38, were obtained by Cox regression and least absolute shrinkage and selection operator (Lasso) regression analyses and to construct a risk model. The OS of high-risk group was lower. And the area under curves (AUCs) of Receiver operating characteristic (ROC) curves were & gt;0.7 at 1, 3, and 5 years. Cox analysis showed that age, grade G3, grade G4, IDH status, ATRX status, BCR status, and risk Scores were reliable independent prognostic factors. In addition, three different immune cells, Mast cells activated, NK cells activated and B cells naive, 24 different HLA family genes, such as HLA-DPA1 and HLA-H, and 8 different immune checkpoints, such as ICOS, LAG3, and CD274, were found between the high and low risk groups. The model genes were significantly relevant with proliferation, cell differentiation, and apoptosis. Conclusion The four genes, PARP9, BST1, NMNAT2, and CD38, might be important molecular biomarkers and therapeutic targets for glioma patients.
    Type of Medium: Online Resource
    ISSN: 2296-875X
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fsurg.2023.1071259
    DOI: 10.3389/fsurg.2023.1071259.s001
    DOI: 10.3389/fsurg.2023.1071259.s002
    DOI: 10.3389/fsurg.2023.1071259.s003
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2773823-1
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  • 7
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    Retinol binding protein 1‐dependent activation of NF‐ κB signaling enhances the malignancy of non‐glioblastomatous diffuse gliomas
    Wiley ; 2022
    In:  Cancer Science Vol. 113, No. 2 ( 2022-02), p. 517-528
    Details
    In: Cancer Science, Wiley, Vol. 113, No. 2 ( 2022-02), p. 517-528
    Abstract: Nonglioblastomatous diffuse glioma (non‐GDG) is a heterogeneous neuroepithelial tumor that exhibits a varied survival range from 4 to 13 years based on the diverse subtypes. Recent studies demonstrated novel molecular markers can predict prognosis for non‐GDG patients; however, these findings as well as pathological classification strategies show obvious limitations on malignant transition due to the heterogeneity among non‐GDGs. Therefore, developing reliable prognostic biomarkers and therapeutic targets have become an urgent need for precisely distinguishing non‐GDG subtypes, illuminating the underlying mechanism. Nuclear factor κβ (NF‐κB) has been proved to be a significant nuclear transcriptional regulator with specific DNA‐binding sequences to participate in multiple pathophysiological processes. However, the underlying mechanism of NF‐κB activation still needs to be further investigated. Herein, our results indicated retinol‐binding protein 1 (RBP1) was significantly upregulated in the IDH WT and 1p19q Non co‐del non‐GDG subtypes and enriched RBP1 expression was markedly correlated with more severe outcomes. Additionally, malignant signatures of the non‐GDG cells including proliferation, migration, invasion, and self‐renewal were significantly suppressed by lentiviral knockdown of RBP1. To further explore the underlying molecular mechanism, bioinformatics analysis was performed using databases, and the results demonstrated RBP1 was strongly correlated with tumor necrosis factor α (TNFα)–NF‐κB signaling. Moreover, exogenous silencing of RBP1 reduced phosphorylation of IkB‐kinase α (IKKα) and thus decreased NF‐κB expression via decreasing the degradation of the IκBα protein. Altogether, these data suggested RBP1‐dependent activation of NF‐κB signaling promoted malignancy of non‐GDG, indicating that RBP1 could be a reliable prognostic biomarker and potential therapeutic target for non‐GDG.
    Type of Medium: Online Resource
    ISSN: 1347-9032 , 1349-7006
    URL: Issue
    URL: Article
    DOI: 10.1111/cas.v113.2
    DOI: 10.1111/cas.15233
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2115647-5
    detail.hit.zdb_id: 2111204-6
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  • 8
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    Data_Sheet_1.pdf
    Frontiers Media SA ; 2020
    In:  Frontiers in Oncology Vol. 10 ( 2020-10-21)
    Details
    In: Frontiers in Oncology, Frontiers Media SA, Vol. 10 ( 2020-10-21)
    Type of Medium: Online Resource
    ISSN: 2234-943X
    URL: Article
    URL: Article
    DOI: 10.3389/fonc.2020.01750
    DOI: 10.3389/fonc.2020.01750.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2020
    detail.hit.zdb_id: 2649216-7
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  • 9
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    Online Resource
    A novel DNA damage and repair‐related gene signature to improve predictive capacity of overall survival for patients with gliomas
    Wiley ; 2022
    In:  Journal of Cellular and Molecular Medicine Vol. 26, No. 13 ( 2022-07), p. 3736-3750
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 26, No. 13 ( 2022-07), p. 3736-3750
    Abstract: Gliomas, as the most lethal and malignant brain tumours in adults, remain a major challenge worldwide. DNA damage and repair‐related genes (DDRRGs) appear to play a significant role in gliomas, but the studies of DDRRGs are still insufficient. Herein, we systematically explored and analysed 1547 DDRRGs in 938 glioma samples from TCGA and CGGA datasets. Using least absolute shrinkage and selection operator (LASSO) Cox regression analysis, we identified a 16‐DDRRG signature, characterized by high‐risk and low‐risk patterns. This risk model harbours robust predictive capability for overall survival of glioma patients. We found the high‐risk score is strongly associated with well‐known malignant features of gliomas, such as the mesenchymal subtype, IDH‐wildtype, 1p/19q non‐codeletion and MGMT promoter unmethylated status. In addition, we found that the high‐risk score is also linked with multiple oncogenic pathways and therapeutic resistance. Significantly, we found the high‐risk group has higher enrichment of immunosuppressive cells (M2‐type macrophages, Tregs and MDSCs) and immune inhibition biomarkers (PD‐1, PD‐L1 and CTLA‐4). Lastly, we proved that SMC4, which has the highest positive regression coefficient in our risk model, is strongly linked with malignant progression and TMZ resistance of gliomas in a E2F1‐dependent manner.
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.v26.13
    DOI: 10.1111/jcmm.17406
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2076114-4
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