Commentary: Geographic Variations in the Incidence of Glioblastoma and Prognostic Factors Predictive of Overall Survival in US Adults from 2004–2013

Mortazavi, S.M.J.

doi:10.3389/fnagi.2018.00105

Cited by 2 publications

(2 citation statements)

References 11 publications

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“…Maximal resection followed by temozolomide (TMZ) and radiation is currently the most optimized treatment regimen that a clinician can use to treat newly diagnosed patients (Karachi et al, 2018;Lacroix et al, 2001). Even with such a regimen, the survival median remains short at between 15 and 18 months with only 10% 5-year survivors (Mortazavi, 2018;Woo et al, 2018). Though the biological behaviors of glioblastoma are characterized by rapid proliferation and aggressive local invasion in CNS, the molecular genetics of glioblastoma remains poorly understood, which impedes the development of more effective treatments.…”

Section: Introductionmentioning

confidence: 99%

PUM2 Promotes Glioblastoma Cell Proliferation and Migration via Repressing BTG1 Expression

Sun

Yang

et al. 2019

Cell Struct. Funct.

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PUM2, an RNA binding protein, is known to promote stem cell proliferation via repressing expressions of cell cycle genes. Similar with stem cells, malignant cells are characterized by unlimited proliferation and remote migration. However, roles of PUM2 in cancer development are controversial. Here, we investigated PUM2's role in glioblastoma development and its relationship with the cell cycle regulator BTG1. Immunoblotting and RT-qPCR were used to evaluate protein expression level and transcript level, respectively. ShRNAs were designed to knock down PUM2 and BTG1 expression. CCK-8 assay was used to evaluate cell viability. Cell migration assay and evasion assay were used to evaluate metastatic capability of glioblastoma cell. RNA pull-down assay and RNA immunoprecipitation assay were used to test the interaction between PUM2 and BTG1 3'UTR. PUM2 expression is elevated in glioblastoma tumor tissues as well as glioblastoma cell lines. PUM2 knockdown remarkably suppresses glioblastoma cell proliferation and migration. In addition, PUM2 knockdown increases BTG1 expression. RNA pull-down assay and RNA immunoprecipitation assay show PUM2 binds to BTG1 3'UTR directly. Furthermore, knockdown of BTG1 reverses the effect of PUM2 knockdown on glioblastoma cell proliferation and migration. Our results suggest that PUM2 promote glioblastoma development via repressing BTG1 expression. declare that they have no conflict of interest.

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Section: Introductionmentioning

confidence: 99%

PUM2 Promotes Glioblastoma Cell Proliferation and Migration via Repressing BTG1 Expression

Sun

Yang

et al. 2019

Cell Struct. Funct.

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“…Glioblastoma (GBM), as the most common primary malignant brain tumor in adults, is one of the most aggressive and lethal human tumors characterized by a block in cellular differentiation. The median survival can range from 12 to 15 months among patients undergoing the current standard of care treatment involving surgery, chemotherapy, and radiation therapy ( Ji et al, 2015 ; Shabihkhani et al, 2017 ; Xu et al, 2017 ; Mortazavi, 2018 ; Jin et al, 2019 ). For GBM patients, the disease is hardly diagnosed in the early stage.…”

Section: Introductionmentioning

confidence: 99%

Identification of signaling pathways associated with achaete-scute homolog 1 in glioblastomas through ChIP-seq data bioinformatics

Zhang

Liu

et al. 2022

Front. Genet.

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Background: Achaete-scute homolog 1 transcription factors were important in the differentiation of neuronal-like glioblastoma (GBM) cancer stem cells (CSCs). To gain a better understanding of the role of ASCL1 in GBM, chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq) data can be analyzed to construct their gene transcription regulation network.Methods: GSE87618 was downloaded from the Gene Expression Omnibus, which is a famous database, in the field of biology. The filtered clean reads were mapped to the human genome utilizing the software of bowtie2. Then, differential peak analysis was performed by diffbind. Finally, the annotated gene functions and signaling pathways were investigated by Gene ontology function and kyoto encyclopedia of genes genomes (KEGG) pathway enrichment analysis. Moreover, the protein–protein interaction network (PPI) analysis of genes obtained from ASCL1 was carried out to explore the hub genes influenced by ASCL1.Results: A total of 516 differential peaks were selected. GO analysis of functions revealed that promoter, untranslated region (UTR), exon, intron, and intergenic genes were mainly enriched in biological pathways such as keratinization, regulation of cAMP metabolic process, blood coagulation, fibrin clot formation, midgut development, and synapse assembly. Genes were mainly enriched in KEGG pathways including pentose phosphate pathway, glycosphingolipid biosynthesis—globo and isoglobo series, ECM–receptor interaction, and adherens junction. In total, 244 nodes and 475 interaction pairs were included in the PPI network with the hub genes including EGFR, CTNNB1, and SPTAN1.Conclusion: EGFR, SPTAN1, and CTNN1B might be the potential down-stream genes of ASCL1 in GBM development, and CTNN1B might make contributions to GBM progression on regulating the cAMP pathway.

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Commentary: Geographic Variations in the Incidence of Glioblastoma and Prognostic Factors Predictive of Overall Survival in US Adults from 2004–2013

Cited by 2 publications

References 11 publications

PUM2 Promotes Glioblastoma Cell Proliferation and Migration via Repressing BTG1 Expression

PUM2 Promotes Glioblastoma Cell Proliferation and Migration via Repressing BTG1 Expression

Identification of signaling pathways associated with achaete-scute homolog 1 in glioblastomas through ChIP-seq data bioinformatics

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