Transcriptome profiles associated with selenium deficiency dependent oxidative stress identify potential diagnostic and therapeutic targets in liver cancer cells
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ABSTRACT:
PROVIDER: PRJNA688308 | ENA |
REPOSITORIES: ENA
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Project description:Hepatocellular carcinoma (HCC) cells show increased resistance to various stress conditions such as oxidative stress. Conventional therapies have low efficacies due to resistance and off-target effects in HCC. Here we aimed to analyze oxidative stress-related gene expression profiles of two HCC cell lines. To identify important genes that cause resistance to reactive oxygen species (ROS), a model of oxidative stress upon selenium (Se) deficiency was utilized in which an affymetrix microarray data was generated for two isogenic HCC cell lines - HepG2 and HepG2-2.2.15 (Head-to-Tail HBV genome integration) that are either sensitive or resistant to Se deficiency dependent oxidative stress, respectively.
2020-12-29 | GSE163950 | GEO
Project description:Hepatocellular carcinoma (HCC) is one of the most common cancer types with high mortality rates and displays increased resistance to various stress conditions such as oxidative stress. Conventional therapies have low efficacies due to resistance and off-target effects in HCC. Here we aimed to analyze oxidative stress-related gene expression profiles of HCC cells and identify genes that could be crucial for novel diagnostic and therapeutic strategies. To identify important genes that cause resistance to reactive oxygen species (ROS), a model of oxidative stress upon selenium (Se) deficiency was utilized. The results of transcriptome-wide gene expression data were analyzed in which the differentially expressed genes (DEGs) were identified between HCC cell lines that are either resistant or sensitive to Se-deficiency-dependent oxidative stress. These DEGs were further investigated for their importance in oxidative stress resistance by network analysis methods, and 27 genes were defined to have key roles; 16 of which were previously shown to have impact on liver cancer patient survival. These genes might have Se-deficiency-dependent roles in hepatocarcinogenesis and could be further exploited for their potentials as novel targets for diagnostic and therapeutic approaches.
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Project description:Selenium deficiency in mice is associated with pro-longevity mechanisms due to reduced amino acid levels and altered nutrient signaling
2019-05-29 | GSE129138 | GEO
Project description:Moderate selenium deficiency may lead to an impaired capacity to cope with health challenges. Functional effects of suboptimal selenium intake are not fully known, and biomarkers for an insufficient selenium supply are inadequate. We therefore fed mice diets of moderately deficient or adequate selenium intake for 6 weeks. Changes in global gene expression were monitored by microarray analysis in splenic leukocytes. Genes for four selenoproteins, Sepw1, Gpx1, Selh and Sep15, were the most significantly down-regulated in moderate selenium deficiency, and this was confirmed by quantitative polymerase chain reaction (qPCR). Classification of significantly affected genes revealed that processes related to inflammation, heme biosynthesis, DNA replication and transcription, cell cycle and transport were affected by selenium restriction. Down-regulation by moderate selenium deficiency of specific genes involved in inflammation and heme biosynthesis was confirmed by qPCR. Myeloperoxidase and lysozyme activities were decreased in selenium-restricted leukocytes, providing evidence for functional consequences. Genes for 31 nuclear factor (NF)-κB targets were down-regulated in moderate selenium deficiency, indicating an impaired NF-κB signaling. Together, the observed changes point to a disturbance in inflammatory response. The selenoproteins found here to be sensitive to selenium intake in murine leukocytes might also be useful as biomarkers for a moderate selenium deficiency in humans.
2018-07-13 | GSE117026 | GEO
Project description:Ferroptosis, a non-apoptotic form of programmed cell death, is triggered by oxidative stress in cancer, heat stress in plants and hemorrhagic stroke. A homeostatic transcriptional response to ferroptotic stimuli is unknown. We show that neurons respond to ferroptotic stress by induction of a transcriptional adaptive response. Pharmacological selenium (Se) augments mitochondrial and nuclear GPX4 and other genes in this transcriptional program, the selenome, via coordinated activation of the transcription factors TFAP2c and Sp1, to protect neurons. This RNA seq data uses primary cortical neurons in cultures treated with either homocysteic acid (HCA), which induces ferroptosis and/or Se, which augments the adaptation to ferroptosis. Both protective (1mM Se) and non-protective (0.1mM Se) of selenium are used. Cells are collected after 6 hours when the transcriptional response is observed.
2019-02-20 | GSE126787 | GEO
Project description:Methanococcus maripaludis utilizes selenocysteine-(Sec-) containing proteins (selenoproteins), mostly active in the organism’s primary energy metabolism, methanogenesis. Under selenium depletion, M. maripaludis employs a set of enzymes containing cysteine (Cys) instead of Sec. The genes coding for these Sec-/Cys-containing isoforms are the only genes known expression of which is influenced by the selenium status of the cell. Using quantitative proteomics and transcriptomics approx. 7% and 12%, respectively, of all genes/proteins were differentially expressed/synthesized in response to the selenium supply. Some of the genes identified involve methanogenesis, nitrogenase functions, and putative transporters. An increase of transcript abundance for putative transporters under selenium-depleted conditions indicated the organism’s effort to tap into alternative sources of selenium. Selenium sources M. maripaludis is known to utilize are selenite and dimethylselenide. To expand this list, a selenium responsive reporter strain was assessed with nine other, environmentally relevant selenium species. While some had a similar biological window as selenite, others were effectively utilized at lower concentrations. Conversely, selenate and seleno-amino acids were only utilized at unphysiologically high concentrations and two compounds were not utilized at all. To address the role of the selenium-regulated putative transporters in selenium transport, M. maripaludis mutant strains lacking one or two of the putative transporters were tested for the capability to utilize the different selenium species. Of the five putative transporters analyzed by loss-of-function mutagenesis, none appeared to be absolutely required for utilizing any of the selenium species tested, indicating they have redundant and/or overlapping specificities, or are not dedicated selenium transporters.
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Project description:Selenium Deficiency is Associated with Pro-Longevity Mechanisms
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Project description:Methylmercury (MeHg) is a well-known neurotoxicant, particularly harmful for the developing brain. Selenium is a nutrient previously shown to interact with MeHg, however the molecular mechanisms behind these interaction is not fully described. To explore the effect of selenium on MeHg, mice were exposed to selenomethionine (SeMet) and MeHg in a 2 x 3 full factorial design for 12 weeks. After termination, organs, including the brain, were collected for Hg and Se analysis. The hippocampus was collected and analysed using gel free proteomics and RNA sequencing (RNA-seq). The presence of SeMet reduced the amount of Hg in several organs, including the brain, while the level of Hg were increased in the feces. The presence of Hg also increased the concentration of selenium in liver and cortex. Proteomic and RNA-seq analyses showed that several known pathways of MeHg toxicity, such as oxidative stress, altered metabolism and calcium disruption were alleviated when SeMet were present. Our results suggest that SeMet can to a certain extent ameliorate the neurotoxic effects of MeHg in a mouse model. Although, whether this is due to decrease of body burden of Hg or through direct interactions with selenium in vivo remains unclear.
2020-08-29 | GSE135381 | GEO
Project description:Genome-wide expression analysis in C. Elegans grown in axenic media with low to toxic selenium concentrations We performed Affymetrix micorarray-based transcriptional profiling on wild-type C. Elegans Bristol N2 grown in low Se axenic media supplemented with five concentrations of selenium, from low to toxic, and harvested at the L4-larva stage.
2014-07-03 | GSE54011 | GEO