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Glioblastoma Microenvironment and Cellular Interactions

Crivii, Carmen-Bianca, Boșca, Adina Bianca, Melincovici, Carmen Stanca, Constantin, Anne-Marie, Mărginean, Mariana, Dronca, Eleonora, Suflețel, Rada, Gonciar, Diana, Bungărdean, Maria, Șovrea, Alina·2022·Cancers
DOI 10.3390/cancers14041092PMC PMC8870579
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Abstract

The central nervous system (CNS) represents a complex network of different cells, such as neurons, glial cells, and blood vessels. In tumor pathology, glial cells result in the highest number of cancers, and glioblastoma (GB) is considered the most lethal tumor in this region. The development of GB leads to the infiltration of healthy tissue through the interaction between all the elements of the brain network. This results in a GB microenvironment, a complex peritumoral hallo composed of tumor cells and several non-tumor cells (e.g., nervous cells, stem cells, fibroblasts, vascular and immune cells), which might be the principal factor for the ineffective treatment due to the fact that the microenvironment modulates the biologic status of the tumor with the increase in its evasion capacity. Crosstalk between glioma cells and the brain microenvironment finally inhibits the beneficial action of molecular pathways, favoring the development and invasion of the tumor and its increasing resistance to treatment. A deeper understanding of cell–cell interactions in the tumor microenvironment (TME) and with the tumor cells could be the basis for a more efficient therapy.

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  1. Verkhratsky, 2018, Physiology of Astroglia, Physiol. Rev., 98, 239, 10.1152/physrev.00042.2016 · DOI · Paper page
  2. Ho, 2019, Editorial: Glia in Health and Disease, Front. Mol. Neurosci., 12, 63, 10.3389/fnmol.2019.00063 · DOI
  3. Kleihues, P., Burger, P.C., and Scheithauer, B.W. (1993). Histological typing of tumours of the central nervous system. World Health Organization International Histological Classification of Tumours, Springer. [2nd ed.]. · DOI
  4. Kleihues, P., and Cavenee, W.K. (2000). World Health Organisation Classification of Tumours: Pathology and Genetics of Tumours of the Nervous System, IARC Press.
  5. Louis, D.N., Ohgaki, H., Wiestler, O.D., and Cavenee, W.K. (2007). WHO Classification of Tumours of the Central Nervous System, IARC Press. [4th ed.]. · DOI
  6. Louis, D.N., Ohgaki, H., Wiestler, O.D., and Cavenee, W.K. (2016). WHO Classification of Tumours of the Central Nervous System, Revise, IARC Press. [4th ed.].
  7. Virtuoso, A., Giovannoni, R., De Luca, C., Gargano, F., Cerasuolo, M., Maggio, N., Lavitrano, M., and Papa, M. (2021). The Glioblastoma Microenvironment: Morphology, Metabolism, and Molecular Signature of Glial Dynamics to Discover Metabolic Rewiring Sequence. Int. J. Mol. Sci., 22. · DOI
  8. Qiu, 2021, Metabolic Remodeling in Glioma Immune Microenvironment: Intercellular Interactions Distinct from Peripheral Tumors, Front. Cell Dev. Biol., 9, 693215, 10.3389/fcell.2021.693215 · DOI
  9. Mostofa, A.G., Punganuru, S.R., Madala, H.R., Al-Obaide, M., and Srivenugopal, K.S. (2017). The Process and Regulatory Components of Inflammation in Brain Oncogenesis. Biomolecules, 7. · DOI
  10. Haksoyler, 2021, Neutrophil-to-lymphocyte ratio is prognostic in recurrent glioblastoma multiforme treated with bevacizumab plus irinotecan, Biomark. Med., 15, 851, 10.2217/bmm-2021-0271 · DOI
  11. Ali, S., Borin, T.F., Piranlioglu, R., Ara, R., Lebedyeva, I., Angara, K., Achyut, B.R., Arbab, A.S., and Rashid, M.H. (2021). Changes in the tumor microenvironment and outcome for TME-targeting therapy in glioblastoma: A pilot study. PLoS ONE, 16. · DOI
  12. Zhang, 2020, Novel insights into astrocyte-mediated signaling of proliferation, invasion and tumor immune microenvironment in glioblastoma, Biomed. Pharmacother., 126, 110086, 10.1016/j.biopha.2020.110086 · DOI
  13. Azambuja, 2020, Molecular profiles and immunomodulatory activities of glioblastoma-derived exosomes, Neurooncol. Adv., 2, vdaa056
  14. Han, 2019, Extracellular vesicles in the tumor microenvironment: Old stories, but new tales, Mol. Cancer, 18, 59, 10.1186/s12943-019-0980-8 · DOI
  15. Gavard, 2017, Spitting out the demons: Extracellular vesicles in glioblastoma, Cell Adh. Migr., 11, 164, 10.1080/19336918.2016.1247145 · DOI
  16. Skog, 2008, Glioblastoma microvesicles transport RNA and proteins that promote tumor growth and provide diagnostic biomarkers, Nat. Cell Biol., 10, 1470, 10.1038/ncb1800 · DOI · Paper page
  17. Harder, 2018, Developments in Blood-Brain Barrier Penetrance and Drug Repurposing for Improved Treatment of Glioblastoma, Front. Oncol., 8, 462, 10.3389/fonc.2018.00462 · DOI
  18. Treps, 2016, Extracellular vesicle-transported Semaphorin3A promotes vascular permeability in glioblastoma, Oncogene, 35, 2615, 10.1038/onc.2015.317 · DOI
  19. Simon, 2018, Shedding of bevacizumab in tumour cells-derived extracellular vesicles as a new therapeutic escape mechanism in glioblastoma, Mol. Cancer, 17, 132, 10.1186/s12943-018-0878-x · DOI
  20. Mondal, 2017, Extracellular Vesicles as Modulators of Tumor Microenvironment and Disease Progression in Glioma, Front. Oncol., 7, 144, 10.3389/fonc.2017.00144 · DOI
  21. Hallal, 2019, Extracellular Vesicles Released by Glioblastoma Cells Stimulate Normal Astrocytes to Acquire a Tumor-Supportive Phenotype Via p53 and MYC Signaling Pathways, Mol. Neurobiol., 56, 4566, 10.1007/s12035-018-1385-1 · DOI
  22. Nareshkumar, 2018, Inhibition of angiogenesis in endothelial cells by Human Lysyl oxidase propeptide, Sci. Rep., 8, 10426, 10.1038/s41598-018-28745-8 · DOI
  23. Fidoamore, 2016, Glioblastoma Stem Cells Microenvironment: The Paracrine Roles of the Niche in Drug and Radioresistance, Stem Cells Int., 2016, 6809105, 10.1155/2016/6809105 · DOI
  24. Treps, 2017, Glioblastoma stem-like cells secrete the pro-angiogenic VEGF-A factor in extracellular vesicles, J. Extracell. Vesicles, 6, 1359479, 10.1080/20013078.2017.1359479 · DOI
  25. Sun, 2017, Glioma stem cells-derived exosomes promote the angiogenic ability of endothelial cells through miR-21/VEGF signal, Oncotarget, 8, 36137, 10.18632/oncotarget.16661 · DOI
  26. Bronisz, 2014, Extracellular vesicles modulate the glioblastoma microenvironment via a tumor suppression signaling network directed by miR-1, Cancer Res., 74, 738, 10.1158/0008-5472.CAN-13-2650 · DOI · Paper page
  27. Kucharzewska, 2013, Exosomes reflect the hypoxic status of glioma cells and mediate hypoxia-dependent activation of vascular cells during tumor development, Proc. Natl. Acad. Sci. USA, 110, 7312, 10.1073/pnas.1220998110 · DOI · Paper page
  28. Svensson, 2011, Hypoxia triggers a proangiogenic pathway involving cancer cell microvesicles and PAR-2-mediated heparin-binding EGF signaling in endothelial cells, Proc. Natl. Acad. Sci. USA, 108, 13147, 10.1073/pnas.1104261108 · DOI · Paper page
  29. Pallini, 2010, Tumour vascularization via endothelial differentiation of glioblastoma stem-like cells, Nature, 468, 824, 10.1038/nature09557 · DOI
  30. Ding, 2021, The relationship between expression of PD-L1 and HIF-1α in glioma cells under hypoxia, J. Hematol. Oncol., 14, 92, 10.1186/s13045-021-01102-5 · DOI
  31. Noronha, C., Ribeiro, A.S., Taipa, R., Castro, D.S., Reis, J., Faria, C., and Paredes, J. (2021). Cadherin Expression and EMT: A Focus on Gliomas. Biomedicines, 9. · DOI
  32. Guan, 2018, Reactive astrocytes in glioblastoma multiforme, Mol. Neurobiol., 55, 6927, 10.1007/s12035-018-0880-8 · DOI
  33. Vinken, 2006, Connexins and their channels in cell growth and cell death, Cell. Signal., 18, 592, 10.1016/j.cellsig.2005.08.012 · DOI
  34. Lim, 2011, Gap junction-mediated import of microRNA from bone marrow stromal cells can elicit cell cycle quiescence in breast cancer cells, Cancer Res., 71, 1550, 10.1158/0008-5472.CAN-10-2372 · DOI
  35. Kar, 2012, Biological role of connexin intercellular channels and hemichannels, Arch. Biochem. Biophys., 524, 2, 10.1016/j.abb.2012.03.008 · DOI
  36. Sinyuk, 2018, Cancer Connectors: Connexins, Gap Junctions, and Communication, Front. Oncol., 8, 646, 10.3389/fonc.2018.00646 · DOI
  37. Osswald, 2015, Brain tumour cells interconnect to a functional and resistant network, Nature, 528, 93, 10.1038/nature16071 · DOI
  38. Weil, 2017, Tumor microtubes convey resistance to surgical lesions and chemotherapy in gliomas, Neuro-Oncology, 19, 1316, 10.1093/neuonc/nox070 · DOI
  39. Soroceanu, 2001, Reduced expression of connexin-43 and functional gap junction coupling in human gliomas, Glia, 33, 107, 10.1002/1098-1136(200102)33:2<107::AID-GLIA1010>3.0.CO;2-4 · DOI
  40. Pu, 2004, Altered expression of Cx43 in astrocytic tumors, Clin. Neurol. Neurosurg., 107, 49, 10.1016/j.clineuro.2004.03.006 · DOI
  41. Bjervig, 1990, Effect of epidermal growth factor on glioma cell growth, migration and invasion in vitro, Cancer Res., 50, 6039
  42. Cottrell, 1998, Regulation of connexin-43 gap junctional intercellular communication by mitogen-activated protein kinase, J. Biol. Chem., 15, 9188
  43. Potthoff, A.L., Heiland, D.H., Evert, B.O., Almeida, F.R., Behringer, S.P., Dolf, A., Güresir, Á., Güresir, E., Joseph, K., and Pietsch, T. (2019). Inhibition of Gap Junctions Sensitizes Primary Glioblastoma Cells for Temozolomide. Cancers, 11. · DOI
  44. Dermietzel, 1993, Gap junctions in the brain: Where, what type, how many and why?, Trends Neurosci., 16, 186, 10.1016/0166-2236(93)90151-B · DOI
  45. Zhang, 1999, Direct gap junction communication between malignant glioma cells and astrocytes, Cancer Res., 59, 1994
  46. Parsons, 2008, An integrated genomic analysis of human glioblastoma multiforme, Science, 321, 1807, 10.1126/science.1164382 · DOI · Paper page
  47. Verkhratsky, 2000, Ion channels in glial cells, Brain Res. Rev., 32, 380, 10.1016/S0165-0173(99)00093-4 · DOI
  48. Molenaar, 2011, Ion channels in glioblastoma, ISRN Neurol., 2011, 590249, 10.5402/2011/590249 · DOI
  49. Ransom, 2001, BK channels in human glioma cells, J. Neurophysiol., 85, 790, 10.1152/jn.2001.85.2.790 · DOI
  50. Ishiuchi, 2002, Blockage of Ca2+-permeable AMPA receptors suppresses migration and induces apoptosis in human glioblastoma cells, Nat. Med., 8, 971, 10.1038/nm746 · DOI
  51. Masi, 2005, hERG1 channels are overexpressed in glioblastoma multiforme and modulate VEGF secretion in glioblastoma cell lines, Br. J. Cancer, 93, 781, 10.1038/sj.bjc.6602775 · DOI
  52. Godard, 2003, Classification of human astrocytic gliomas on the basis of gene expression: A correlated group of genes with angiogenic activity emerges as a strong predictor of subtypes, Cancer Res., 63, 6613
  53. Yan, 2009, IDH1 and IDH2 mutations in gliomas, N. Engl. J. Med., 360, 765, 10.1056/NEJMoa0808710 · DOI · Paper page
  54. Joshi, 2011, Sodium ion channel mutations in glioblastoma patients correlate with shorter survival, Mol. Cancer, 10, 17, 10.1186/1476-4598-10-17 · DOI
  55. Iser, 2019, EMT-like process in glioblastomas and reactive astrocytes, Neurochem. Int., 122, 139, 10.1016/j.neuint.2018.11.016 · DOI
  56. Dongre, 2019, New insights into the mechanisms of epithelial-mesenchymal transition and implications for cancer, Nat. Rev. Mol. Cell Biol., 20, 69, 10.1038/s41580-018-0080-4 · DOI · Paper page
  57. Hara, 2021, Interactions between cancer cells and immune cells drive transitions to mesenchymal-like states in glioblastoma, Cancer Cell, 39, 779, 10.1016/j.ccell.2021.05.002 · DOI
  58. Lee, 2006, The epithelial-mesenchymal transition: New insights in signaling, development, and disease, J. Cell Biol., 172, 973, 10.1083/jcb.200601018 · DOI
  59. Iwadate, 2016, Epithelial-mesenchymal transition in glioblastoma progression, Oncol. Lett., 11, 1615, 10.3892/ol.2016.4113 · DOI
  60. Pez, 2011, The HIF-1-inducible lysyl oxidase activates HIF-1 via the Akt pathway in a positive regulation loop and synergizes with HIF-1 in promoting tumor cell growth, Cancer Res., 71, 1647, 10.1158/0008-5472.CAN-10-1516 · DOI
  61. Kalluri, 2009, The basics of epithelial-mesenchymal transition, J. Clin. Investig., 119, 1420, 10.1172/JCI39104 · DOI · Paper page
  62. Yu, 2014, Cancer-associated fibroblasts induce epithelial-mesenchymal transition of breast cancer cells through paracrine TGF-β signaling, Br. J. Cancer, 110, 724, 10.1038/bjc.2013.768 · DOI
  63. Bierie, 2006, Tumor microenvironment: TGFbeta: The molecular Jekyll and Hyde of cancer, Nat. Rev. Cancer, 6, 506, 10.1038/nrc1926 · DOI
  64. Ye, 2012, Tumor-associated microglia/macrophages enhance the invasion of glioma stem-like cells via TGF-β1 signaling pathway, J. Immunol., 189, 444, 10.4049/jimmunol.1103248 · DOI
  65. Nieto, 2016, EMT: 2016, Cell, 166, 21, 10.1016/j.cell.2016.06.028 · DOI · Paper page
  66. Kahlert, 2012, Activation of canonical WNT/β-catenin signaling enhances in vitro motility of glioblastoma cells by activation of ZEB1 and other activators of epithelial-to-mesenchymal transition, Cancer Lett., 325, 42, 10.1016/j.canlet.2012.05.024 · DOI
  67. Siebzehnrubl, 2013, The ZEB1 pathway links glioblastoma initiation, invasion and chemoresistance, EMBO Mol. Med., 5, 1196, 10.1002/emmm.201302827 · DOI
  68. Lu, 2012, VEGF inhibits tumor cell invasion and mesenchymal transition through a MET/VEGFR2 complex, Cancer Cell, 22, 21, 10.1016/j.ccr.2012.05.037 · DOI
  69. Piao, 2012, Glioblastoma resistance to anti-VEGF therapy is associated with myeloid cell infiltration, stem cell accumulation, and a mesenchymal phenotype, Neuro-Oncology, 14, 1379, 10.1093/neuonc/nos158 · DOI
  70. Cooper, 2012, The tumor microenvironment strongly impacts master transcriptional regulators and gene expression class of glioblastoma, Am. J. Pathol., 180, 2108, 10.1016/j.ajpath.2012.01.040 · DOI
  71. Koch, 2016, Reciprocal regulation of the cholinic phenotype and epithelial-mesenchymal transition in glioblastoma cells, Oncotarget, 7, 73414, 10.18632/oncotarget.12337 · DOI
  72. Cano, 2000, The transcription factor snail controls epithelial-mesenchymal transitions by repressing E-cadherin expression, Nat. Cell Biol., 2, 76, 10.1038/35000025 · DOI
  73. Thiery, 2002, Epithelial-mesenchymal transitions in tumour progression, Nat. Rev. Canc., 2, 442, 10.1038/nrc822 · DOI
  74. Hulpiau, 2009, Molecular evolution of the cadherin superfamily, Int. J. Biochem. Cell Biol., 41, 349, 10.1016/j.biocel.2008.09.027 · DOI
  75. Majc, 2020, Epithelial-to-mesenchymal transition as the driver of changing carcinoma and glioblastoma microenvironment, Biochim. Biophys. Acta Mol. Cell Res., 1867, 118782, 10.1016/j.bbamcr.2020.118782 · DOI
  76. Iser, 2017, The Epithelial-to-Mesenchymal Transition-Like Process in Glioblastoma: An Updated Systematic Review and In Silico Investigation, Med. Res. Rev., 37, 271, 10.1002/med.21408 · DOI
  77. Iser, 2016, Conditioned Medium from Adipose-Derived Stem Cells (ADSCs) Promotes Epithelial-to-Mesenchymal-Like Transition (EMT-Like) in Glioma Cells In vitro, Mol. Neurobiol., 53, 7184, 10.1007/s12035-015-9585-4 · DOI
  78. Shimoyama, 2000, Identification of three human type-II classic cadherins and frequent heterophilic interactions between different subclasses of type-II classic cadherins, Biochem. J., 349, 159, 10.1042/bj3490159 · DOI
  79. Noh, M.G., Oh, S.J., Ahn, E.J., Kim, Y.J., Jung, T.Y., Jung, S., Kim, K.K., Lee, J.H., Lee, K.H., and Moon, K.S. (2017). Prognostic significance of E-cadherin and N-cadherin expression in Gliomas. BMC Cancer, 17. · DOI
  80. Wu, 2013, Expression of beta-catenin and E- and N-cadherin in human brainstem gliomas and clinicopathological correlations, Int. J. Neurosci., 123, 318, 10.3109/00207454.2012.758123 · DOI
  81. Lewis-Tuffin, L.J., Rodriguez, F., Giannini, C., Scheithauer, B., Necela, B.M., Sarkaria, J.N., and Anastasiadis, P.Z. (2010). Misregulated E-cadherin expression associated with an aggressive brain tumor phenotype. PLoS ONE, 5. · DOI
  82. Camand, 2012, N-cadherin expression level modulates integrin-mediated polarity and strongly impacts on the speed and directionality of glial cell migration, J. Cell Sci., 125, 844, 10.1242/jcs.087668 · DOI
  83. Asano, 2004, Correlation of N-cadherin expression in high grade gliomas with tissue invasion, J. Neurooncol., 70, 3, 10.1023/B:NEON.0000040811.14908.f2 · DOI
  84. Utsuki, 2012, Adult cerebellar glioblastoma cases have different characteristics from supratentorial glioblastoma, Brain Tumor Pathol., 29, 87, 10.1007/s10014-011-0070-0 · DOI
  85. Verhaak, 2010, Cancer Genome Atlas Research Network. Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1, Cancer Cell, 17, 98, 10.1016/j.ccr.2009.12.020 · DOI · Paper page
  86. Ravi, 2019, Tumor-associated reactive astrocytes aid the evolution of immunosuppressive environment in glioblastoma, Nat. Commun., 10, 2541, 10.1038/s41467-019-10493-6 · DOI · Paper page
  87. Zong, 2012, The cellular origin for malignant glioma and prospects for clinical advancements, Expert Rev. Mol. Diagn., 12, 383, 10.1586/erm.12.30 · DOI
  88. Katz, A.M., Amankulor, N.M., Pitter, K., Helmy, K., Squatrito, M., and Holland, E.C. (2012). Astrocyte-specific expression patterns associated with the PDGF-induced glioma microenvironment. PLoS ONE, 7. · DOI
  89. Matias, 2018, Microglia/Astrocytes-Glioblastoma Crosstalk: Crucial Molecular Mechanisms and Microenvironmental Factors, Front. Cell Neurosci., 12, 235, 10.3389/fncel.2018.00235 · DOI
  90. Irvin, 2017, Intrinsic Astrocyte Heterogeneity Influences Tumor Growth in Glioma Mouse Models, Brain Pathol., 27, 36, 10.1111/bpa.12348 · DOI
  91. Parmigiani, 2021, Old Stars and New Players in the Brain Tumor Microenvironment, Front. Cell Neurosci., 15, 709917, 10.3389/fncel.2021.709917 · DOI
  92. Gril, 2013, Pazopanib inhibits the activation of PDGFRβ-expressing astrocytes in the brain metastatic microenvironment of breast cancer cells, Am. J. Pathol., 182, 2368, 10.1016/j.ajpath.2013.02.043 · DOI
  93. Amit, 2015, Paracrine regulation of glioma cells invasion by astrocytes is mediated by glial- derived neurotrophic factor, Int. J. Cancer, 137, 1012, 10.1002/ijc.29380 · DOI
  94. Rempel, 1998, SPARC: A signal of astrocytic neoplastic transformation and reactive response in human primary and xenograft gliomas, J. Neuropathol. Exp. Neurol., 57, 1112, 10.1097/00005072-199812000-00002 · DOI
  95. Liddelow, 2017, Reactive Astrocytes: Production, Function, and Therapeutic Potential, Immunity, 46, 957, 10.1016/j.immuni.2017.06.006 · DOI · Paper page
  96. Laird, 2008, Opposing roles for reactive astrocytes following traumatic brain injury, Neurosignals, 16, 154, 10.1159/000111560 · DOI
  97. Buffo, 2008, Origin and progeny of reactive gliosis: A source of multipotent cells in the injured brain, Proc. Natl. Acad. Sci. USA, 105, 3581, 10.1073/pnas.0709002105 · DOI
  98. Robel, 2011, The stem cell potential of glia: Lessons from reactive gliosis, Nat. Rev. Neurosci., 12, 88, 10.1038/nrn2978 · DOI
  99. Garcia, 2004, GFAP-expressing progenitors are the principal source of constitutive neurogenesis in adult mouse forebrain, Nat. Neurosci., 7, 1233, 10.1038/nn1340 · DOI
  100. Lang, 2004, Astrocytes in injured adult rat spinal cord may acquire the potential of neural stem cells, Neuroscience, 128, 775, 10.1016/j.neuroscience.2004.06.033 · DOI
  101. Wisniewski, 2016, Tumour-processed osteopontin and lactadherin drive the protumorigenic reprogramming of microglia and glioma progression, Oncogene, 35, 6366, 10.1038/onc.2016.55 · DOI
  102. Turkowski, 2018, VEGF as a modulator of the innate immune response in glioblastoma, Glia, 66, 161, 10.1002/glia.23234 · DOI
  103. Laudati, 2017, Blockade of CCR5 receptor prevents M2 microglia phenotype in a microglia-glioma paradigm, Neurochem. Int., 108, 100, 10.1016/j.neuint.2017.03.002 · DOI
  104. Rickert, U., Grampp, S., Wilms, H., Spreu, J., Knerlich-Lukoschus, F., Held-Feindt, J., and Lucius, R. (2014). Glial cell line-derived neurotrophic factor family members reduce microglial activation via inhibiting p38MAPKs-mediated inflammatory responses. J. Neurodegener. Dis., 369468. · DOI
  105. Kim, 2017, The role of the tumor microenvironment in glioblastoma: A mathematical model, IEEE Trans. Biomed. Eng., 64, 519
  106. Ghosh, 2018, Bioenergetic regulation of microglia, Glia, 66, 1200, 10.1002/glia.23271 · DOI
  107. Pellerin, 2013, Unraveling the complex metabolic nature of astrocytes, Front. Cell. Neurosci., 7, 179
  108. Kros, 2014, Circulating glioma biomarkers, Neuro-Oncology, 17, 343
  109. Okolie, 2016, Reactive astrocytes potentiate tumor aggressiveness in a murine glioma resection and recurrence model, Neuro-Oncology, 18, 1622, 10.1093/neuonc/now117 · DOI
  110. Schiffer, D., Annovazzi, L., Casalone, C., Corona, C., and Mellai, M. (2018). Glioblastoma: Microenvironment and Niche Concept. Cancers, 11. · DOI
  111. Silver, 2013, Chondroitin sulfate proteoglycans potently inhibit invasion and serve as a central organizer of the brain tumor microenvironment, J. Neurosci., 33, 15603, 10.1523/JNEUROSCI.3004-12.2013 · DOI
  112. Eder, 2015, The Dynamics of Interactions among Immune and Glioblastoma Cells, Neuromol. Med., 17, 335, 10.1007/s12017-015-8362-x · DOI
  113. Kim, 2015, Macitentan, a Dual Endothelin Receptor Antagonist, in Combination with Temozolomide Leads to Glioblastoma Regression and Long-term Survival in Mice, Clin. Cancer Res., 21, 4630, 10.1158/1078-0432.CCR-14-3195 · DOI
  114. Imai, 2013, Epigenetic transcriptional activation of monocyte chemotactic protein 3 contributes to long-lasting neuropathic pain, Brain, 136, 828, 10.1093/brain/aws330 · DOI
  115. Jackson, 2018, Regulation of mitochondrial dynamics in astrocytes: Mechanisms, consequences, and unknowns, Glia, 66, 1213, 10.1002/glia.23252 · DOI
  116. Jackson, 2016, Transient Oxygen/Glucose Deprivation Causes a Delayed Loss of Mitochondria and Increases Spontaneous Calcium Signaling in Astrocytic Processes, J. Neurosci., 36, 7109, 10.1523/JNEUROSCI.4518-15.2016 · DOI
  117. Woods, 1999, The AMP-activated protein kinase is involved in the regulation of ketone body production by astrocytes, J. Neurochem., 73, 1674, 10.1046/j.1471-4159.1999.731674.x · DOI
  118. Seyfried, 2015, Metabolic therapy: A new paradigm for managing malignant brain cancer, Cancer Lett., 356, 289, 10.1016/j.canlet.2014.07.015 · DOI
  119. Goldberg, 2002, Gap junctions between cells expressing connexin 43 or 32 show inverse permselectivity to adenosine and ATP, J. Biol. Chem., 277, 36725, 10.1074/jbc.M109797200 · DOI
  120. Gagliano, 2009, Glioma-astrocyte interaction modifies the astrocyte phenotype in a co-culture experimental model, Oncol. Rep., 22, 1349, 10.3892/or_00000574 · DOI
  121. Barbero, 2002, Expression of the chemokine receptor CXCR4 and its ligand stromal cell-derived factor 1 in human brain tumors and their involvement in glial proliferation in vitro, Ann. N. Y. Acad. Sci., 973, 60, 10.1111/j.1749-6632.2002.tb04607.x · DOI
  122. Kim, 2014, Tumoral RANKL activates astrocytes that promote glioma cell invasion through cytokine signaling, Cancer Lett., 353, 194, 10.1016/j.canlet.2014.07.034 · DOI
  123. Clement, 2007, HEDGEHOG-GLI1 signaling regulates human glioma growth, cancer stem cell self-renewal, and tumorigenicity, Curr. Biol., 17, 165, 10.1016/j.cub.2006.11.033 · DOI
  124. Biasoli, 2014, Glioblastoma cells inhibit astrocytic p53-expression favoring cancer malignancy, Oncogenesis, 3, e123, 10.1038/oncsis.2014.36 · DOI
  125. Chen, 2013, Extracellular matrix proteins regulate epithelial-mesenchymal transition in mammary epithelial cells, Differentiation, 86, 126, 10.1016/j.diff.2013.03.003 · DOI
  126. Piperi, C., Papavassiliou, K.A., and Papavassiliou, A.G. (2019). Pivotal Role of STAT3 in Shaping Glioblastoma Immune Microenvironment. Cells, 8. · DOI
  127. Suzuki, 2010, Higher pAkt expression predicts a significant worse prognosis in glioblastomas, J. Radiat. Res., 51, 343, 10.1269/jrr.09109 · DOI
  128. Seike, 2011, Interaction between lung cancer cells and astrocytes via specific inflammatory cytokines in the microenvironment of brain metastasis, Clin. Exp. Metastasis, 28, 13, 10.1007/s10585-010-9354-8 · DOI
  129. DeBerardinis, 2007, Beyond aerobic glycolysis: Transformed cells can engage in glutamine metabolism that exceeds the requirement for protein and nucleotide synthesis, Proc. Natl. Acad. Sci. USA, 104, 19345, 10.1073/pnas.0709747104 · DOI · Paper page
  130. Sin, 2016, Astrocytes promote glioma invasion via the gap junction protein connexin43, Oncogene, 35, 1504, 10.1038/onc.2015.210 · DOI
  131. Le, 2003, Exploitation of astrocytes by glioma cells to facilitate invasiveness: A mechanism involving matrix metalloproteinase-2 and the urokinase-type plasminogen activator-plasmin cascade, J. Neurosci., 23, 4034, 10.1523/JNEUROSCI.23-10-04034.2003 · DOI
  132. Li, 2010, IL-6 augments the invasiveness of U87MG human glioblastoma multiforme cells via up-regulation of MMP-2 and fascin-1, Oncol. Rep., 23, 1553, 10.3892/or_00000795 · DOI
  133. Huang, 2010, Extracellular matrix of glioblastoma inhibits polarization and transmigration of T cells: The role of tenascin-C in immune suppression, J. Immunol., 185, 1450, 10.4049/jimmunol.0901352 · DOI
  134. Qi, 2016, IL-10 secreted by M2 macrophage promoted tumorigenesis through interaction with JAK2 in glioma, Oncotarget, 7, 71673, 10.18632/oncotarget.12317 · DOI
  135. Zhang, 2009, Stat3 inhibition activates tumor macrophages and abrogates glioma growth in mice, Glia, 57, 1458, 10.1002/glia.20863 · DOI
  136. Gabrilovich, 2009, Myeloid-derived suppressor cells as regulators of the immune system, Nat. Rev. Immunol., 9, 162, 10.1038/nri2506 · DOI · Paper page
  137. Nefedova, 2004, Hyperactivation of STAT3 is involved in abnormal differentiation of dendritic cells in cancer, J. Immunol., 172, 464, 10.4049/jimmunol.172.1.464 · DOI · Paper page
  138. Chen, 2016, Carcinoma-astrocyte gap junctions promote brain metastasis by cGAMP transfer, Nature, 533, 493, 10.1038/nature18268 · DOI · Paper page
  139. Placone, 2016, The role of astrocytes in the progression of brain cancer: Complicating the picture of the tumor microenvironment, Tumor Biol., 37, 61, 10.1007/s13277-015-4242-0 · DOI
  140. Mega, 2020, Astrocytes enhance glioblastoma growth, Glia, 68, 316, 10.1002/glia.23718 · DOI
  141. Lin, 2016, Astrocytes protect glioma cells from chemotherapy and upregulate survival genes via gap junctional communication, Mol. Med. Rep., 13, 1329, 10.3892/mmr.2015.4680 · DOI
  142. Zhang, 2019, Chemoresistance caused by the microenvironment of glioblastoma and the corresponding solutions, Biomed. Pharmacother., 109, 39, 10.1016/j.biopha.2018.10.063 · DOI
  143. Hong, 2015, Gap junctions modulate glioma invasion by direct transfer of microRNA, Oncotarget, 6, 15566, 10.18632/oncotarget.3904 · DOI
  144. Rath, 2015, Coculture with astrocytes reduces the radiosensitivity of glioblastoma stem-like cells and identifies additional targets for radiosensitization, Cancer Med., 4, 1705, 10.1002/cam4.510 · DOI
  145. Kao, 2007, Inhibition of phosphatidylinositol-3-OH kinase/Akt signaling impairs DNA repair in glioblastoma cells following ionizing radiation, J. Biol. Chem., 282, 21206, 10.1074/jbc.M703042200 · DOI
  146. Yu, 2017, Identification of diverse astrocyte populations and their malignant analogs, Nat. Neurosci., 20, 396, 10.1038/nn.4493 · DOI · Paper page
  147. Venkatesh, 2015, Neuronal Activity Promotes Glioma Growth through Neuroligin-3 Secretion, Cell, 161, 803, 10.1016/j.cell.2015.04.012 · DOI
  148. Sundar, 2014, The role of cancer stem cells in glioblastoma, Neurosurg. Focus, 37, E6, 10.3171/2014.9.FOCUS14494 · DOI
  149. Yu, 2008, Pluripotent stem cell lines, Genes Dev., 22, 1987, 10.1101/gad.1689808 · DOI
  150. Tang, 2012, Understanding cancer stem cell heterogeneity and plasticity, Cell Res., 22, 457, 10.1038/cr.2012.13 · DOI
  151. Prasetyanti, 2017, Intra-tumor heterogeneity from a cancer stem cell perspective, Mol. Cancer, 16, 41, 10.1186/s12943-017-0600-4 · DOI
  152. Najafi, 2019, Cancer stem cell (CSC) resistance drivers, Life Sci., 234, 116781, 10.1016/j.lfs.2019.116781 · DOI
  153. Deshpande, 2015, Cancer Stem Cells: Formidable Allies of Cancer, Indian J. Surg. Oncol., 6, 400, 10.1007/s13193-015-0451-7 · DOI
  154. Piper, 2021, Glioma Stem Cells as Immunotherapeutic Targets: Advancements and Challenges, Front. Oncol., 11, 615704, 10.3389/fonc.2021.615704 · DOI
  155. Gimple, 2019, Glioblastoma stem cells: Lessons from the tumor hierarchy in a lethal cancer, Genes Dev., 33, 591, 10.1101/gad.324301.119 · DOI · Paper page
  156. Eun, 2017, Cancer stem cell heterogeneity: Origin and new perspectives on CSC targeting, BMB Rep., 50, 117, 10.5483/BMBRep.2017.50.3.222 · DOI
  157. Wang, 2019, Stem cells in tissues, organoids, and cancers, Cell Mol. Life Sci., 76, 4043, 10.1007/s00018-019-03199-x · DOI
  158. Feinberg, 2006, The epigenetic progenitor origin of human cancer, Nat. Rev. Genet., 7, 21, 10.1038/nrg1748 · DOI
  159. Lerner, 2014, Asymmetric cell division of stem and progenitor cells during homeostasis and cancer, Cell. Mol. Life Sci., 71, 575, 10.1007/s00018-013-1386-1 · DOI
  160. Singh, 2004, Identification of human brain tumour initiating cells, Nature, 432, 396, 10.1038/nature03128 · DOI
  161. Calabrese, 2007, A perivascular niche for brain tumor stem cells, Cancer Cell, 11, 69, 10.1016/j.ccr.2006.11.020 · DOI
  162. Lee, 2018, Human glioblastoma arises from subventricular zone cells with low-level driver mutations, Nature, 560, 243, 10.1038/s41586-018-0389-3 · DOI · Paper page
  163. Mondal, 2018, Nutritional stress reprograms dedifferention in glioblastoma multiforme driven by PTEN/Wnt/Hedgehog axis: A stochastic model of cancer stem cells, Cell Death Discov., 4, 110, 10.1038/s41420-018-0126-6 · DOI
  164. Lathia, 2015, Cancer stem cells in glioblastoma, Genes Dev., 29, 1203, 10.1101/gad.261982.115 · DOI · Paper page
  165. Rosińska, S., and Gavard, J. (2021). Tumor Vessels Fuel the Fire in Glioblastoma. Int. J. Mol. Sci., 22. · DOI
  166. Garnier, 2019, Glioblastoma Stem-Like Cells, Metabolic Strategy to Kill a Challenging Target, Front. Oncol., 9, 118, 10.3389/fonc.2019.00118 · DOI
  167. Prager, 2020, Glioblastoma Stem Cells: Driving Resilience through Chaos, Trends Cancer, 6, 223, 10.1016/j.trecan.2020.01.009 · DOI · Paper page
  168. Tang, 2021, Targeting Glioblastoma Stem Cells: A Review on Biomarkers, Signal Pathways and Targeted Therapy, Front. Oncol., 11, 701291, 10.3389/fonc.2021.701291 · DOI
  169. Alves, 2021, Role of glioblastoma stem cells in cancer therapeutic resistance: A perspective on antineoplastic agents from natural sources and chemical derivatives, Stem Cell Res. Ther., 12, 206, 10.1186/s13287-021-02231-x · DOI
  170. Brescia, P., Richichi, C., and Pelicci, G. (2012). Current strategies for identification of glioma stem cells: Adequate or unsatisfactory?. J. Oncol., 376894. · DOI
  171. Xu, 2017, Cancer stem cell markers in glioblastoma—An update, Eur. Rev. Med. Pharmacol. Sci., 21, 3207
  172. Lombard, 2021, The Subventricular Zone; A Hideout for Adult and Pediatric High-Grade Glioma Stem Cells, Front. Oncol., 10, 614930, 10.3389/fonc.2020.614930 · DOI
  173. Wang, 2021, The adaptive transition of glioblastoma stem cells and its implications on treatments, Sig. Transduct. Target. Ther., 6, 124, 10.1038/s41392-021-00491-w · DOI
  174. Pinto, 2021, Patient-derived glioblastoma stem cells transfer mitochondria through tunneling nanotubes in tumor organoids, Biochem. J., 478, 21, 10.1042/BCJ20200710 · DOI
  175. Ho, 2017, Contribution of the Microenvironmental Niche to Glioblastoma Heterogeneity, Biomed. Res. Int., 2017, 9634172, 10.1155/2017/9634172 · DOI
  176. Roehlecke, C., and Schmidt, M.H.H. (2020). Tunneling Nanotubes and Tumor Microtubes in Cancer. Cancers, 12. · DOI
  177. Wei, 2020, Cellular and Extracellular Components in Tumor Microenvironment and Their Application in Early Diagnosis of Cancers, Anal. Cell. Pathol., 2020, 6283796, 10.1155/2020/6283796 · DOI
  178. Chen, 2021, Role of microRNAs in glioblastoma, Oncotarget, 12, 1707, 10.18632/oncotarget.28039 · DOI · Paper page
  179. Wu, 2021, Adaptive Mechanisms of Tumor Therapy Resistance Driven by Tumor Microenvironment, Front. Cell Dev. Biol., 9, 641469, 10.3389/fcell.2021.641469 · DOI
  180. Auffinger, 2015, The role of glioma stem cells in chemotherapy resistance and glioblastoma multiforme recurrence, Expert Rev. Neurother., 15, 741, 10.1586/14737175.2015.1051968 · DOI
  181. Iwadate, 2018, Plasticity in Glioma Stem Cell Phenotype and Its Therapeutic Implication, Neurol. Med. Chir., 58, 61, 10.2176/nmc.ra.2017-0089 · DOI
  182. Baisiwala, S., Auffinger, B., Caragher, S.P., Shireman, J.M., Ahsan, R., Lee, G., Hasan, T., Park, C., Saathoff, M.R., and Christensen, A.C. (2019). Chemotherapeutic Stress Induces Transdifferentiation of Glioblastoma Cells to Endothelial Cells and Promotes Vascular Mimicry. Stem Cells Int., 6107456. · DOI
  183. Șovrea, A.S., Boșca, B., Melincovici, C.S., Constantin, A.-M., Crintea, A., Mărginean, M., Dronca, E., Jianu, M.E., Suflețel, R., and Gonciar, D. (2022). Multiple Faces of the Glioblastoma Microenvironment. Int. J. Mol. Sci., 23. · DOI · Paper page
  184. Hu, 2015, Microglial and macrophage polarization—New prospects for brain repair, Nat. Rev. Neurol., 11, 56, 10.1038/nrneurol.2014.207 · DOI · Paper page
  185. Markovic, 2005, Microglia stimulate the invasiveness of glioma cells by increasing the activity of metalloprotease-2, J. Neuropathol. Exp. Neurol., 64, 754, 10.1097/01.jnen.0000178445.33972.a9 · DOI
  186. Markovic, 2011, Minocycline reduces glioma expansion and invasion by attenuating microglial MT1-MMP expression, Brain. Behav. Immun., 25, 624, 10.1016/j.bbi.2011.01.015 · DOI
  187. Zhai, 2011, Microglia/macrophages promote glioma progression, Glia, 59, 472, 10.1002/glia.21117 · DOI
  188. Pires-Afonso, Y., Niclou, S.P., and Michelucci, A. (2020). Revealing and Harnessing Tumour-Associated Microglia/Macrophage Heterogeneity in Glioblastoma. Int. J. Mol. Sci., 21. · DOI
  189. Poon, 2019, Differential microglia and macrophage profiles in human IDH-mutant and -wild type glioblastoma, Oncotarget, 10, 3129, 10.18632/oncotarget.26863 · DOI
  190. Chen, 2018, Immune Microenvironment in Glioblastoma Subtypes, Front. Immunol., 9, 1004, 10.3389/fimmu.2018.01004 · DOI
  191. Hambardzumyan, 2016, The role of microglia and macrophages in glioma maintenance and progression, Nat. Neurosci., 19, 20, 10.1038/nn.4185 · DOI · Paper page
  192. Ochocka, 2021, Single-cell RNA sequencing reveals functional heterogeneity of glioma-associated brain macrophages, Nat. Commun., 12, 1151, 10.1038/s41467-021-21407-w · DOI
  193. Roesch, S., Rapp, C., Dettling, S., and Herold-Mende, C. (2018). When Immune Cells Turn Bad-Tumor-Associated Microglia/Macrophages in Glioma. Int. J. Mol. Sci., 19. · DOI
  194. Wei, 2019, Osteopontin mediates glioblastoma-associated macrophage infiltration and is a potential therapeutic target, Clin. Investig., 129, 137, 10.1172/JCI121266 · DOI
  195. Hutter, 2019, Microglia are effector cells of CD47-SIRPα antiphagocytic axis disruption against glioblastoma, Proc. Natl. Acad. Sci. USA, 116, 997, 10.1073/pnas.1721434116 · DOI
  196. Cribaro, 2020, Phagocytic glioblastoma-associated microglia and macrophages populate invading pseudopalisades, Brain Commun., 2, fcz043, 10.1093/braincomms/fcz043 · DOI
  197. Ma, 2021, Mutant IDH1 promotes phagocytic function of microglia/macrophages in gliomas by downregulating ICAM1, Cancer Lett., 517, 35, 10.1016/j.canlet.2021.05.038 · DOI
  198. Brandenburg, S., Blank, A., Bungert, A.D., and Vajkoczy, P. (2020). Distinction of Microglia and Macrophages in Glioblastoma: Close Relatives, Different Tasks?. Int. J. Mol. Sci., 22. · DOI
  199. Venteicher, 2017, Decoupling genetics, lineages, and microenvironment in IDH-mutant gliomas by single-cell RNA-seq, Science, 355, eaai8478, 10.1126/science.aai8478 · DOI
  200. Friebel, 2020, Single-Cell Mapping of Human Brain Cancer Reveals Tumor-Specific Instruction of Tissue-Invading Leukocytes, Cell, 181, 1626, 10.1016/j.cell.2020.04.055 · DOI

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Metadata

Authors
Crivii, C.-B., Boșca, A. B., Melincovici, C. S., Constantin, A.-M., Mărginean, M., Dronca, E., Suflețel, R., Gonciar, D., Bungărdean, M., & Șovrea, A.
Affiliations
  • Anatomy and Embryology Discipline, Morphological Sciences Department, Iuliu Hațieganu University of Medicine and Pharmacy, 400000 Cluj-Napoca, Romania
  • Histology Discipline, Morphological Sciences Department, Iuliu Hațieganu University of Medicine and Pharmacy, 400000 Cluj-Napoca, Romania
  • Medical Genetics Discipline, Molecular Sciences Department, Iuliu Hațieganu University of Medicine and Pharmacy, 400000 Cluj-Napoca, Romania
  • Pathological Anatomy Discipline, Morphological Sciences Department, Iuliu Hațieganu University of Medicine and Pharmacy, 400000 Cluj-Napoca, Romania
ORCID
Crivii, Carmen-Bianca
Venue
Cancers
Publisher
MDPI AG
Published
2022-02-21
Volume
14
Issue
4
Pages
1092
ISSN
2072-6694
DOI
10.3390/cancers14041092
PMC
PMC8870579
Cited by
81
References
17
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)

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