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Gene expression analyses of GSC11 cell in stem cell culture conditions or in differentiation conditions for 1, 3, or 7 days

ABSTRACT: Although fetal bovine serum (FBS) induces the differentiation of cancer stem cells, the underlying mechanism by which this is accomplished has not been clarified. Whether reactive oxygen species affect the differentiation of cancer stem cells in solid tumors as they do in normal stem cells is not known. This study aimed to determine the role of reactive oxygen species in the FBS-induced differentiation of glioblastoma stem cells. We found that FBS activated the oxidative stress response system in glioblastoma stem cells (GSCs). The resulting differentiated cells showed tremendous increases in mitochondrial superoxide and oxygen consumption, accompanied by a loss in stem cell markers and a gain in differentiation markers. The antioxidant N-Acetyl-Cysteine (NAC) inhibited the mitochondrial superoxide increase and prevented the glioblastoma stem cells from differentiating. It appears that FBS-induced cancer stem cell differentiation is caused by mitochondrial activation, which depends on increases in levels of mitochondrial superoxide. GSC11 cells were cultured in stem cell medium or differentiated medium for 1, 3, or 7 days in triplicate. Total RNA was extracted from 12 samples. Microarray experiment and data analysis were done at Dept. of Systems Biology, MDACC (Houston, USA)

ORGANISM(S): Homo sapiens

SUBMITTER: Sangbae Kim

PROVIDER: E-GEOD-28220 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression analyses of GSC11 cell in stem cell culture conditions or in differentiation conditions for 1, 3, or 7 days

Project description:Although fetal bovine serum (FBS) induces the differentiation of cancer stem cells, the underlying mechanism by which this is accomplished has not been clarified. Whether reactive oxygen species affect the differentiation of cancer stem cells in solid tumors as they do in normal stem cells is not known. This study aimed to determine the role of reactive oxygen species in the FBS-induced differentiation of glioblastoma stem cells. We found that FBS activated the oxidative stress response system in glioblastoma stem cells (GSCs). The resulting differentiated cells showed tremendous increases in mitochondrial superoxide and oxygen consumption, accompanied by a loss in stem cell markers and a gain in differentiation markers. The antioxidant N-Acetyl-Cysteine (NAC) inhibited the mitochondrial superoxide increase and prevented the glioblastoma stem cells from differentiating. It appears that FBS-induced cancer stem cell differentiation is caused by mitochondrial activation, which depends on increases in levels of mitochondrial superoxide.

2015-02-27 | GSE28220 | GEO

Switch of mitochondrial superoxide dismutase into a prooxidant peroxidase in manganese-deficient cells

Project description:Superoxide radical anion and other Reactive Oxygen Species are constantly produced during respiration. In mitochondria, the dismutation of the superoxide radical anion is accelerated by the mitochondrial superoxide dismutase 2 (SOD2), an enzyme that has been traditionally associated with antioxidant protection. However, increases in SOD2 expression promote oxidative stress, indicating that there may be a prooxidant role for SOD2. We show that SOD2, which normally binds manganese, can incorporate iron and generate an alternative isoform with peroxidase activity. The switch from manganese to iron allows FeSOD2 to utilize H2O2 to promote oxidative stress. We found that FeSOD2 is formed in cultured cells. FeSOD2 causes mitochondrial dysfunction and higher levels of oxidative stress in cultured cells. We show that formation of FeSOD2 converts an antioxidant defense into a prooxidant peroxidase that leads to cellular changes seen in multiple human diseases.

2017-12-05 | GSE106206 | GEO

Transcription profiling of Arabidopis leaves from plants treated with antimycin A to trigger mitochondrial production of reactive oxygen species

Project description:mitochondrial electron transport in Arabidopsis leaves was blocked by antimycin A treatment to trigger mitochondrial production of reactive oxygen species and to study transcriptional changes in response

2010-12-31 | E-TABM-641 | biostudies-arrayexpress

Antimycin A treatment of Arabidopsis leaves in a PrxII F knockout

Project description:Mitochondrial electron transport in Arabidopsis leaves was blocked by antimycin A treatment to trigger mitochondrial production of reactive oxygen species in a knockout line for a mitochondrial peroxidase (PrxII F) and to study transcriptional changes in response

2011-11-01 | E-TABM-1196 | biostudies-arrayexpress

Gene expression profiles between mtROShigh and mtROSlow cells dissociated from E14.5 neocortical cells were compared by microarray

Project description:sample collection protocol:We used FACS to separate the E14.5 neocortical cells into high mitochondrial reactive oxygen species (mtROS) and low mitochondrial ROS cell populations and compared their expression profiles. Transition of progenitors through progressive stages of differentiation probably involves dynamic changes in mtROS levels, depending on the needs of the cell. We found that the progenitors had higher levels of mtROS, but these levels significantly decreased with differentiation.

2017-03-30 | E-MTAB-5438 | biostudies-arrayexpress

Reactive oxygen species (ROS) production activates unconventional secretion of antioxidant proteins

Project description:Signal-sequence-lacking superoxide dismutase 1 (SOD1) is secreted upon nutrient starvation, but the physiological relevance of this secretion is unclear. We now report that secreted SOD1 is functionally active. In addition, a secretome analysis has revealed number of other secreted cytoplasmic antioxidant enzymes, including both thioredoxins, (Trx1 and Trx2), and the peroxiredoxin Ahp1. Our data reveal that starvation triggers increased mitochondrial activity, leading to increased production of reactive oxygen species (ROS). Inhibiting mitochondrial activity or ROS, inhibited secretion of the antioxidants. We suggest elevated ROS that evade cytoplasmic antioxidants, can permeate across the plasma membrane to the extracellular space. Cells secrete antioxidants to prevent ROS-mediated damage to the extracellular space. These findings thus provide an understanding of why cells secrete signal sequence lacking proteins like SOD1 and the larger family of antioxidants.

2019-05-14 | PXD010849 | Pride

Accumulated α-synuclein affects the progression of GM2 gangliosidoses

Project description:The accumulation of α-synuclein (ASyn) has been observed in several lysosomal storage diseases (LSD), but it remains unclear if the accumulation of ASyn contributes to the pathology. The mitochondria degeneration, reduced expression of manganese superoxide dismutase 2, and reactive oxygen species-mediated oxidative damage were observed in the neurons of Hexb-/- mice. Gene expression in the brain of 14-week-old Hexb-/- ASyn+/+, Hexb-/- Asyn-Tg, and Hexb-/- ASyn-/- mice were analyzed.

2015-05-12 | E-GEOD-68748 | biostudies-arrayexpress

A bioenergetic shift is required for spermatogonial differentiation

Project description:A bioenergetic balance between glycolysis and mitochondrial respiration is particularly important for stem cell fate specification. It however remains to be determined whether undifferentiated spermatogonia switch their preference of bioenergy production during differentiation. In this study, we found that ATP generation in spermatogonia was gradually increased upon retinoic acid-induced differentiation. To accommodate this elevated energy demand, retinoic acid signaling concomitantly switched ATP production in spermatogonia from glycolysis to mitochondrial respiration, accompanied by increased levels of reactive oxygen species. In addition, inhibition of glucose conversion to glucose-6-phosphate or pentose phosphate pathway blocked the formation of c-Kit+ differentiating germ cells, suggesting that metabolites produced from glycolysis are required for spermatogonial differentiation. We further demonstrated that the expression levels of several metabolic regulators and enzymes were significantly altered upon retinoic acid-induced differentiation by both RNA-seq analyses and quantitative proteomics. Taken together, our data unveil a critically regulated bioenergetic balance between glycolysis and mitochondrial respiration which is required for spermatogonial proliferation and differentiation.

2021-09-09 | PXD019136 | Pride

Fluorescence imaging sheds light on the immune evasion mechanisms of hepatic stellate cells mediated by superoxide anion

Project description:Whether and how the reactive oxygen species generated by hepatic stellate cells (HSCs) promote immune evasion of hepatocellular carcinoma (HCC) remains mysteriouss. Therefore, investigating the function of superoxide anion, the firstly generated reactive oxygen species, during the immune evasion become necessary. In this work, we establish a novel in situ imaging method for visualization of superoxide anion changes in HSCs based on a new two-photon fluorescence probe TPH. TPH comprises recognition group for superoxide anion and HSCs targeting peptides. We observe that superoxide anion in HSCs gradually rose, impairing the infiltration of CD8+ T cells in HCC mice. Further studies reveal that the cyclin-dependent kinase 4 is deactivated by superoxide anion, and then cause the up-regulation of PD-L1. Our work provides molecular insights into HSC-mediated immune evasion of HCC, which may represent potential targets for HCC immunotherapy.

2024-04-08 | PXD051328 |

Mitochondrial Transfer Regulates Cell Fate Through Metabolic Remodeling in Osteoporosis

Project description:Mitochondria are the powerhouse of eukaryotic cells, which regulate cell metabolism and differentiation. Recently, mitochondrial transfer between cells has been shown to direct recipient cell fate. However, it is unclear whether mitochondria can translocate to stem cells and whether this transfer alters stem cell fate. Here, we examined mesenchymal stem cell (MSC) regulation by macrophages in the bone marrow environment. We found that macrophages promote osteogenic differentiation of MSCs by delivering mitochondria to MSCs. However, under osteoporotic conditions, macrophages with altered phenotypes and metabolic statuses release oxidatively damaged mitochondria. The transfer of dysfunctional mitochondria to MSCs triggers a reactive oxygen species burst, which leads to metabolic remodeling. We showed that abnormal metabolism in MSCs is caused by the abnormal succinate accumulation, which is a key factor in abnormal osteogenic differentiation. These results reveal that mitochondrial transfer from macrophages to MSCs allows metabolic crosstalk to regulate bone homeostasis. This mechanism identifies a potential target for the treatment of osteoporosis.

2022-09-11 | GSE198806 | GEO

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