Role of inflammation and oxidative stress mediators in gliomas

Alfredo Conti, Carlo Gulì, Domenico La Torre, Chiara Tomasello, Filippo F Angileri, M'hammed Aguennouz, Alfredo Conti, Carlo Gulì, Domenico La Torre, Chiara Tomasello, Filippo F Angileri, M'hammed Aguennouz

Abstract

Gliomas are the most common primary brain tumors of the central nervous system. Despite relevant progress in conventional treatments, the prognosis of such tumors remains almost invariably dismal. The genesis of gliomas is a complex, multistep process that includes cellular neoplastic transformation, resistance to apoptosis, loss of control of the cell cycle, angiogenesis, and the acquisition of invasive properties. Among a number of different biomolecular events, the existence of molecular connections between inflammation and oxidative stress pathways and the development of this cancer has been demonstrated. In particular, the tumor microenvironment, which is largely orchestrated by inflammatory molecules, is an indispensable participant in the neoplastic process, promoting proliferation, survival and migration of such tumors. Proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin-1beta, and interferon-gamma, as well as chemokines and prostaglandins, are synthesized by resident brain cells and lymphocytes invading the affected brain tissue. Key mediators of cancer progression include nuclear factor-kappaB, reactive oxygen and nitrogen species, and specific microRNAs. The collective activity of these mediators is largely responsible for a pro-tumorigenic response through changes in cell proliferation, cell death, cellular senescence, DNA mutation rates, DNA methylation and angiogenesis. We provide a general overview of the connection between specific inflammation and oxidative stress pathway molecules and gliomas. The elucidation of specific effects and interactions of these factors may provide the opportunity for the identification of new target molecules leading to improved diagnosis and treatment.

Figures

Figure 1
Figure 1
NF-κB DNA-binding activity studied in normal brain tissue and human gliomas with different grade of malignancy. Representative electromobility shift assay autoradiographs showing NF-κB DNA-binding activity studied in normal brain tissue and human gliomas with different grade of malignancy and demonstrating an increased activity in tumor samples that is remarkable in high grade tumors. NBT: normal brain tissue; LGA: low-grade glioma; AA: anaplastic astrocytoma; GBM: glioblastoma multiform; PC: positive control.
Figure 2
Figure 2
Schematic drawing showing the TNF-driven survival and apoptosis balance. TNF signaling induces controlled cell death through the caspase activation cascade. This is counteracted by a survival pathway acting through a TRAF2-driven and NF-kB-mediated transcription of antiapoptotic proteins including members of the c-IAP family (c-IAP1 and 2 and Survivin) acting on the effector caspases 3 and 7 or members of the Bcl-2 family acting on the mitochondrial apoptotic pathway by blocking the release of cytochrome c. TNFR = tumor necrosis factor receptor; TRADD = TNFR associated death domain; FADD = FAS associating protein with death domain.
Figure 3
Figure 3
Possible IL-6-mediated paracrine activation of glioma cells. Schematic drawing describing the hypothesis that inflammatory cells, such as activated macrophage/microglial cells, synthesize IL-6 through NF-κB. As a consequence, glioma cells, particularly tumor stem cells, are activated by IL-6 via paracrine stimulation. Chemokines, including IL-6 and TNFα, activate the transcription factors STAT3 and NF-κB that, in turn, initiate specific pathways for tumor progression such as angiogenesis, migration, and apoptosis inhibition.
Figure 4
Figure 4
Cytokines-related activation of intracellular processes in glioma cells. Glioma specimens were hybridized in a GeneChip microarrays panel of the whole human genome containing approximately 44000 genes. The scheme presented results from statistical analysis as displayed by Gene Spring GX 7.3 software (personal, unpublished data).
Figure 5
Figure 5
Schematic representation of the conversion of arachidonic acid to prostaglandins and other prostanoids.
Figure 6
Figure 6
A possible interaction between environmental and genetic factors in gliomagenesis. Mediators of inflammation and oxidative stress pathways interacts with oncogenes and tumor suppressor genes influencing the evolution toward neoplastic phenotype by unbalancing the DNA repair/damage equilibrium.

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Source: PubMed

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