Detection of Metabolic Change in Glioblastoma Cells after Radiotherapy Using Hyperpolarized 13C-MRI

Dynamic nuclear polarization‐magnetic resonance imaging chemical shift imaging with hyperpolarized [1‐13C] pyruvate was conducted to evaluate the metabolic change in glycolytic profiles after radiation of two glioma stem‐like cell‐derived gliomas and an adherent human glioblastoma cell line in an orthotopic xenograft mouse model.
[Nmr in Biomedicine]
Kawai, T., Brender, J. R., Lee, J. A., Kramp, T., Kishimoto, S., Krishna, M. C., Tofilon, P., & Camphausen, K. A. (n.d.). Detection of metabolic change in glioblastoma cells after radiotherapy using hyperpolarized 13C-MRI. NMR in Biomedicine, n/a(n/a), e4514. https://doi.org/https://doi.org/10.1002/nbm.4514 Cite
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MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44

Transient overexpression of miR-138 in glioblastoma cells inhibited cell proliferation, cell cycle, migration, and wound healing capability.The authors unveiled that miR-138 negatively regulated the expression of CD44 by directly binding to the 3′ UTR of CD44.
[Scientific Reports]
Yeh, M., Wang, Y.-Y., Yoo, J. Y., Oh, C., Otani, Y., Kang, J. M., Park, E. S., Kim, E., Chung, S., Jeon, Y.-J., Calin, G. A., Kaur, B., Zhao, Z., & Lee, T. J. (2021). MicroRNA-138 suppresses glioblastoma proliferation through downregulation of CD44. Scientific Reports, 11(1), 9219. https://doi.org/10.1038/s41598-021-88615-8 Cite
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Global Phosphoproteomics Reveals DYRK1A Regulates CDK1 Activity in Glioblastoma Cells

Both tumor suppressive and oncogenic functions have been reported for dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A). Investigators performed a detailed investigation to delineate the role of DYRK1A in glioblastoma.
[Cell Death Discovery]
Recasens, A., Humphrey, S. J., Ellis, M., Hoque, M., Abbassi, R. H., Chen, B., Longworth, M., Needham, E. J., James, D. E., Johns, T. G., Day, B. W., Kassiou, M., Yang, P., & Munoz, L. (2021). Global phosphoproteomics reveals DYRK1A regulates CDK1 activity in glioblastoma cells. Cell Death Discovery, 7(1), 1–16. https://doi.org/10.1038/s41420-021-00456-6 Cite
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PI3Kγ Inhibition Suppresses Microglia/TAM Accumulation in Glioblastoma Microenvironment to Promote Exceptional Temozolomide Response

Glioblastoma-associated microglia/macrophages secreted interleukin 11 activated STAT3-MYC signaling in glioblastoma cells. This signaling induced stem cell states that conferred enhanced tumorigenicity and resistance to the standard-of-care chemotherapy, temozolomide.
[Proceedings of the National Academy of Sciences of the United States of America]
Li, J., Kaneda, M. M., Ma, J., Li, M., Shepard, R. M., Patel, K., Koga, T., Sarver, A., Furnari, F., Xu, B., Dhawan, S., Ning, J., Zhu, H., Wu, A., You, G., Jiang, T., Venteicher, A. S., Rich, J. N., Glass, C. K., … Chen, C. C. (2021). PI3Kγ inhibition suppresses microglia/TAM accumulation in glioblastoma microenvironment to promote exceptional temozolomide response. Proceedings of the National Academy of Sciences, 118(16). https://doi.org/10.1073/pnas.2009290118 Cite
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Tumor Cell Plasticity, Heterogeneity, and Resistance in Crucial Microenvironmental Niches in Glioma

Scientists identified NOTCH1 as a central switch between the perivascular niche and network niche in glioma, and demonstrated robust cross-compensation when only one niche was targeted.
[Nature Communications]
Jung, E., Osswald, M., Ratliff, M., Dogan, H., Xie, R., Weil, S., Hoffmann, D. C., Kurz, F. T., Kessler, T., Heiland, S., von Deimling, A., Sahm, F., Wick, W., & Winkler, F. (2021). Tumor cell plasticity, heterogeneity, and resistance in crucial microenvironmental niches in glioma. Nature Communications, 12(1), 1014. https://doi.org/10.1038/s41467-021-21117-3 Cite
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SOX1 Is a Backup Gene for Brain Neurons and Glioma Stem Cell Protection and Proliferation

The authors collate the most important discoveries relating to the neuroprotective effects of SOX1 in brain cancer and propose hypothesis worthy of SOX1’s role in the survival of senescent neuronal cells, its roles in fibroblast cell proliferation, and cell fate for neuroprotection, and the discharge of electrical impulses for homeostasis.
[Molecular Neurobiology]
Kanwore, K., Guo, X., Abdulrahman, A. A., Kambey, P. A., Nadeem, I., & Gao, D. (2021). SOX1 Is a Backup Gene for Brain Neurons and Glioma Stem Cell Protection and Proliferation. Molecular Neurobiology. https://doi.org/10.1007/s12035-020-02240-6 Cite
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Modulation of Nogo Receptor 1 Expression Orchestrates Myelin-Associated Infiltration of Glioblastoma

Investigators adopted a radiogenomic analysis to screen for functionally relevant genes that orchestrated the process of glioma cell infiltration through myelin and promoted glioblastoma aggressiveness.
[Brain]
Hong, J.-H., Kang, S., Sa, J. K., Park, G., Oh, Y. T., Kim, T. H., Yin, J., Kim, S. S., D’Angelo, F., Koo, H., You, Y., Park, S., Kwon, H. J., Kim, C. I., Ryu, H., Lin, W., Park, E. J., Kim, Y.-J., Park, M.-J., … Park, J. B. (2021). Modulation of Nogo receptor 1 expression orchestrates myelin-associated infiltration of glioblastoma. Brain, awaa408. https://doi.org/10.1093/brain/awaa408 Cite
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ADO/Hypotaurine: A Novel Metabolic Pathway Contributing to Glioblastoma Development

The authors identified hypotaurine as one of the top-ranked metabolites for differentiating low- and high-grade tumors, and that there was also a strong association between the levels of intratumoral hypotaurine and expression of its biosynthetic enzyme, cysteamine (2-aminoethanethiol) dioxygenase.
[Cell Death Discovery]
Shen, D., Tian, L., Yang, F., Li, J., Li, X., Yao, Y., Lam, E. W.-F., Gao, P., Jin, B., & Wang, R. (2021). ADO/hypotaurine: a novel metabolic pathway contributing to glioblastoma development. Cell Death Discovery, 7(1), 1–11. https://doi.org/10.1038/s41420-020-00398-5 Cite
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Histone Demethylase KDM4C Controls Tumorigenesis of Glioblastoma by Epigenetically Regulating p53 and C-Myc

Researchers showed that KDM4C knockdown significantly repressed proliferation and tumorigenesis of glioblastoma cells in vitro and in vivo that were rescued by overexpressing wild-type KDM4C but not a catalytic dead mutant.
[Cell Death & Disease]
Lee, D. H., Kim, G. W., Yoo, J., Lee, S. W., Jeon, Y. H., Kim, S. Y., Kang, H. G., Kim, D.-H., Chun, K.-H., Choi, J., & Kwon, S. H. (2021). Histone demethylase KDM4C controls tumorigenesis of glioblastoma by epigenetically regulating p53 and c-Myc. Cell Death & Disease, 12(1), 1–14. https://doi.org/10.1038/s41419-020-03380-2 Cite
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Integrated Genetic and Metabolic Landscapes Predict Vulnerabilities of Temozolomide Resistant Glioblastoma Cells

Differential metabolism was identified in response to temozolomide at varying concentrations in both the resistant neurospheroidal and the susceptible glioblastoma cell-lines.
[npj Systems Biology and Applications]
Immanuel, S. R. C., Ghanate, A. D., Parmar, D. S., Yadav, R., Uthup, R., Panchagnula, V., & Raghunathan, A. (2021). Integrated genetic and metabolic landscapes predict vulnerabilities of temozolomide resistant glioblastoma cells. Npj Systems Biology and Applications, 7(1), 1–10. https://doi.org/10.1038/s41540-020-00161-7 Cite
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Tumor Cell Network Integration in Glioma Represents a Stemness Feature

Glioblastoma cells that are part of the tumor microtube-connected tumor network showed activated neurodevelopmental and glioma progression gene expression pathways. Importantly, many of them revealed profiles indicative of increased cellular stemness, including high expression of nestin.
[Neuro-Oncology]
Xie, R., Kessler, T., Grosch, J., Hai, L., Venkataramani, V., Huang, L., Hoffmann, D. C., Solecki, G., Ratliff, M., Schlesner, M., Wick, W., & Winkler, F. (2020). Tumor cell network integration in glioma represents a stemness feature. Neuro-Oncology, noaa275. https://doi.org/10.1093/neuonc/noaa275 Cite
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