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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HIF1α/HIF2α–Sox2/Klf4 Promotes the Malignant Progression of Glioblastoma via the EGFR–PI3K/AKT Signaling Pathway with Positive Feedback under Hypoxia

Scientists discovered that glioblastoma cells exhibited features indicative of malignant progression and were present in a hypoxic environment.
[Cell Death & Disease]
HIF1α/HIF2α–Sox2/Klf4 promotes the malignant progression of glioblastoma via the EGFR–PI3K/AKT signalling pathway with positive feedback under hypoxia | Cell Death & Disease. (n.d.). Retrieved March 24, 2021, from https://www.nature.com/articles/s41419-021-03598-8 Cite
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Cancer-Specific Loss of TERT Activation Sensitizes Glioblastoma to DNA Damage

The authors demonstrated increased binding of a specific GA binding protein B1L (GABPB1L)-isoform–containing complex to the mutant telomerase reverse transcriptase (TERT) promoter. They found that TERT promoter mutant glioblastoma cells, unlike wild-type cells, exhibited a critical near-term dependence on GABPB1L for proliferation.
[Proceedings of the National Academy of Sciences of the United States of America]
Amen, A. M., Fellmann, C., Soczek, K. M., Ren, S. M., Lew, R. J., Knott, G. J., Park, J. E., McKinney, A. M., Mancini, A., Doudna, J. A., & Costello, J. F. (2021). Cancer-specific loss of TERT activation sensitizes glioblastoma to DNA damage. Proceedings of the National Academy of Sciences, 118(13). https://doi.org/10.1073/pnas.2008772118 Cite
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Cyclin-Dependent Kinase Inhibitors Exert Distinct Effects on Patient-Derived 2D and 3D Glioblastoma Cell Culture Models

Investigators describe the antitumoral potential of selective cyclin-dependent kinase inhibitors on low-passage glioblastoma multiforme 2D- and 3D models, cultured as neurospheres or glioma stem-like cells.
[Cell Death Discovery]
Riess, C., Koczan, D., Schneider, B., Linke, C., del Moral, K., Classen, C. F., & Maletzki, C. (2021). Cyclin-dependent kinase inhibitors exert distinct effects on patient-derived 2D and 3D glioblastoma cell culture models. Cell Death Discovery, 7(1), 1–15. https://doi.org/10.1038/s41420-021-00423-1 Cite
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CDK1 Is Up-Regulated by Temozolomide in an NF-κB Dependent Manner in Glioblastoma

While cyclin-dependent kinase 1 (CDK1) phosphorylation is a well-described consequence of temozolomide (TMZ) treatment, researchers found that TMZ also robustly induced CDK1 expression.
[Scientific Reports]
Voce, D. J., Bernal, G. M., Cahill, K. E., Wu, L., Mansour, N., Crawley, C. D., Campbell, P.-A. S., Arina, A., Weichselbaum, R. R., & Yamini, B. (2021). CDK1 is up-regulated by temozolomide in an NF-κB dependent manner in glioblastoma. Scientific Reports, 11(1), 5665. https://doi.org/10.1038/s41598-021-84912-4 Cite
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Hsa_circ_0110757 Upregulates ITGA1 to Facilitate Temozolomide Resistance in Glioma by Suppressing Hsa-miR-1298-5p

The role of hsa_circ_0110757 in temozolomide (TMZ)-resistant glioma was evaluated both in vitro and in vivo. It was found that hsa_circ_0110757 and ITGA1 were more highly expressed in TMZ-resistant glioma than in TMZ-sensitive glioma.
[Cell Death & Disease]
Li, H., Liu, Q., Chen, Z., Wu, M., Zhang, C., Su, J., Li, Y., & Zhang, C. (2021). Hsa_circ_0110757 upregulates ITGA1 to facilitate temozolomide resistance in glioma by suppressing hsa-miR-1298-5p. Cell Death & Disease, 12(3), 1–12. https://doi.org/10.1038/s41419-021-03533-x Cite
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Cannabidiol Inhibits Human Glioma by Induction of Lethal Mitophagy Through Activating TRPV4

Researchers investigated the molecular mechanisms underlying the antitumor effect of cannabidiol in preclinical models of human glioma.
[Autophagy]
Huang, T., Xu, T., Wang, Y., Zhou, Y., Yu, D., Wang, Z., He, L., Chen, Z., Zhang, Y., Davidson, D., Dai, Y., Hang, C., Liu, X., & Yan, C. (2021). Cannabidiol inhibits human glioma by induction of lethal mitophagy through activating TRPV4. Autophagy. https://www.tandfonline.com/doi/abs/10.1080/15548627.2021.1885203 Cite
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Dopamine Receptor Antagonists, Radiation, and Cholesterol Biosynthesis in Mouse Models of Glioblastoma

Treatment of glioma cells with the dopamine receptor antagonist quetiapine reduced glioma cell self-renewal in vitro and combined treatment of mice with quetiapine and radiation prolonged the survival of glioma-bearing mice.
[JNCI-Journal of the National Cancer institute]
Bhat, K., Saki, M., Cheng, F., He, L., Zhang, L., Ioannidis, A., Nathanson, D., Tsang, J., Bensinger, S. J., Nghiemphu, P. L., Cloughesy, T. F., Liau, L. M., Kornblum, H. I., & Pajonk, F. (2021). Dopamine Receptor Antagonists, Radiation, and Cholesterol Biosynthesis in Mouse Models of Glioblastoma. JNCI: Journal of the National Cancer Institute, djab018. https://doi.org/10.1093/jnci/djab018 Cite
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Regulation of Tumor Immune Suppression and Cancer Cell Survival by CXCL1/2 Elevation in Glioblastoma Multiforme

Scientists showed that elevation of CXCL1 or CXCL2 facilitated myeloid cell migration and simultaneously disrupted CD8+ T cell accumulation at tumor sites, causing accelerated tumor progression.
[Science Advances]
Hu, J., Zhao, Q., Kong, L.-Y., Wang, J., Yan, J., Xia, X., Jia, Z., Heimberger, A. B., & Li, S. (2021). Regulation of tumor immune suppression and cancer cell survival by CXCL1/2 elevation in glioblastoma multiforme. Science Advances, 7(5), eabc2511. https://doi.org/10.1126/sciadv.abc2511 Cite
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Late p65 Nuclear Translocation in Glioblastoma Cells Indicates Non-Canonical TLR4 Signaling and Activation of DNA Repair Genes

Scientists analyzed Toll-like receptor 4 (TLR4) expression in different grades of astrocytoma, and observed increased expression in tumors, mainly in glioblastoma, compared to non-neoplastic brain tissue.
[Scientific Reports]
Moretti, I. F., Lerario, A. M., Trombetta-Lima, M., Sola, P. R., da Silva Soares, R., Oba-Shinjo, S. M., & Marie, S. K. N. (2021). Late p65 nuclear translocation in glioblastoma cells indicates non-canonical TLR4 signaling and activation of DNA repair genes. Scientific Reports, 11(1), 1333. https://doi.org/10.1038/s41598-020-79356-1 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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