Mechanistic investigations indicated that TGF-β acted on cancer cells to induce the core cancer stem cell-related genes CD133, SOX2, NESTIN, MUSASHI1 and ALDH1A expression and spheres formation via NF-κB–IL6–STAT3 signaling pathway, resulting in the increased cancer stemness and tumorigenic potential.
[Cancer Immunology Immunotherapy]
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Regulatory T cells promote glioma cell stemness through TGF-β–NF-κB–IL6–STAT3 signaling | SpringerLink. (n.d.). Retrieved February 17, 2021, from https://link.springer.com/article/10.1007%2Fs00262-021-02872-0 Cite
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.
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.
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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
Investigators summarize the impact of hypoxia and acidic stress on glioma stem cell signaling and biologic phenotypes, and potential methods to inhibit these pathways.
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The authors report that growth differentiation factor 15 (GDF15) promotes the glioma stem cell (GSC)-like phenotype in GSC-like cells through the activation of leukemia inhibitor factor (LIF)–STAT3 signaling.
[Cell Death Discovery]
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The authors consider how knowledge of E3 ligase biology may be used for future therapeutic interventions in glioblastoma, including the use of blood-brain barrier permeable proteolysis targeting chimeras.
[Cell Death & Differentiation]
The authors utilized glioblastoma neurospheres that display glioblastoma stem cells characteristics and found activation of the PI3K/AKT pathway in sphere-forming cells. The PI3Kα selective inhibitor alpelisib blocked PI3K/AKT activation and inhibited spheroid growth, suggesting an essential role for the PI3Kα catalytic isoform.
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In a hypoxic microenvironment the hypoxia-inducible factor 1α (HIF1α)/HIF2α-miR210-3p network promoted the malignant progression of glioblastoma through a positive feedback loop with epidermal growth factor (EGF).
[Cell Death & Disease]
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The HIF1α/HIF2α-miR210-3p network regulates glioblastoma cell proliferation, dedifferentiation and chemoresistance through EGF under hypoxic conditions | Cell Death & Disease. (n.d.). Retrieved November 18, 2020, from https://www.nature.com/articles/s41419-020-03150-0 Cite
Scientists explored the mechanisms by which lncRNA derived from hypoxic glioma stem cells cause glioma progression. Isolation and identification of the Linc01060 gene, the exosomes containing them, and the proteins from tumor cells regulating the gene allowed for studying the effects of Linc01060 on proliferation and glycometabolism.
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Li, J., Liao, T., Liu, H., Yuan, H., Ouyang, T., Wang, J., Chai, S., Li, J., Chen, J., Li, X., Zhao, H., & Xiong, N. (2020). Hypoxic glioma stem cell-derived exosomes containing Linc01060 promote progression of glioma by regulating the MZF1/c-Myc/HIF-1α. Cancer Research. https://doi.org/10.1158/0008-5472.CAN-20-2270 Cite
Researchers showed that the Special AT‐rich Binding Protein‐2 (SATB2), one of crucial NMPs, recruited histone acetyltransferase CBP to promote the FOXM1‐mediated cell proliferation and tumor growth of glioblastoma.
[EMBO Molecular Medicine]
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Tao, W., Zhang, A., Zhai, K., Huang, Z., Huang, H., Zhou, W., Huang, Q., Fang, X., Prager, B. C., Wang, X., Wu, Q., Sloan, A. E., Ahluwalia, M. S., Lathia, J. D., Yu, J. S., Rich, J. N., & Bao, S. (2020). SATB2 drives glioblastoma growth by recruiting CBP to promote FOXM1 expression in glioma stem cells. EMBO Molecular Medicine, n/a(n/a), e12291. https://doi.org/10.15252/emmm.202012291 Cite
Researchers identified Tenascin C (TNC) to be upregulated and secreted in mesenchymal glioblastoma subtype with high NF-κB signaling activity. Silencing TNC decreased proliferation, migration and suppresses self-renewal of glioma stem cells.