
Glioma cells are resistant to inflammation‑induced alterations of mitochondrial dynamics
Author(s) -
Wange Fan,
Yanan Song,
Zongyao Ren,
Xiaoli Cheng,
Pu Li,
Haiyan Song,
Ling Jia
Publication year - 2020
Publication title -
international journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.405
H-Index - 122
ISSN - 1019-6439
DOI - 10.3892/ijo.2020.5134
Subject(s) - proinflammatory cytokine , glioma , biology , microbiology and biotechnology , inflammation , mitochondrion , downregulation and upregulation , microglia , cancer research , immunology , biochemistry , gene
Accumulating evidence suggests that inammation is present in solid tumors. However, it is poorly understood whether inflammation exists in glioma and how it affects the metabolic signature of glioma. By analyzing immunohistochemical data and gene expression data downloaded from bioinformatic datasets, the present study revealed an accumulation of inflammatory cells in glioma, activation of microglia, upregulation of proinflammatory factors (including IL‑6, IL‑8, hypoxia‑inducible factor‑1α, STAT3, NF‑κB1 and NF‑κB2), destruction of mitochondrial structure and altered expression levels of electron transfer chain complexes and metabolic enzymes. By monitoring glioma cells following proinflammatory stimulation, the current study observed a remodeling of their mitochondrial network via mitochondrial fission. More than half of the mitochondria presented ring‑shaped or spherical morphologies. Transmission electron microscopic analyses revealed mitochondrial swelling with partial or total cristolysis. Furthermore, proinflammatory stimuli resulted in increased generation of reactive oxygen species, decreased mitochondrial membrane potential and reprogrammed metabolism. The defective mitochondria were not eliminated via mitophagy. However, cell viability was not affected, and apoptosis was decreased in glioma cells after proinflammatory stimuli. Overall, the present findings suggested that inflammation may be present in glioma and that glioma cells may be resistant to inflammation‑induced mitochondrial dysfunction.