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Transcriptome analysis for CT mRNA treated BT-549 cells and negative control cells

ABSTRACT: We report the altered metabolite changes by processing CT mRNA in the TNBC cell line, BT-549. It was confirmed that the treatment of CT mRNA disrupted the synthesis of dTTP during nucleic acid metabolism, increasing the signal related to DNA damage in the cell, and that the energy metabolism and NADPH metabolism in the cell were changed for its recovery. The main energy sources, glucose metabolism and glutamine metabolism, are closely linked to the mitochondrial TCA cycle products. In the CT mRNA treatment group, intracellular nucleic acid depletion was observed to increase glutamine metabolism as a source of N source, and the pathway of aspartate utilization was observed. It was confirmed that it was expanded. As a result, a significant increase in the cysteine influx was observed according to the occurrence of ROS, and an effort to regulate the intracellular NADPH balance was observed through the change of metabolites over time. Finally, it was observed that the oncogenic pathway was significantly reduced in the CT mRNA-treated group compared with all untreated groups or controls with other substrate specificities. This study characterizes changes in intracellular metabolites caused by specific dTTP biosynthesis disturbances.

ORGANISM(S): Homo sapiens

PROVIDER: GSE202194 | GEO | 2022/05/07

REPOSITORIES: GEO

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Transcriptome analysis for CT mRNA treated MDA-MB-468 cells and negative control cells

Project description:We report the altered metabolite changes by processing CT mRNA in the TNBC cell line, MDA-MB-468. It was confirmed that the treatment of CT mRNA disrupted the synthesis of dTTP during nucleic acid metabolism, increasing the signal related to DNA damage in the cell, and that the energy metabolism and NADPH metabolism in the cell were changed for its recovery. The main energy sources, glucose metabolism and glutamine metabolism, are closely linked to the mitochondrial TCA cycle products. In the CT mRNA treatment group, intracellular nucleic acid depletion was observed to increase glutamine metabolism as a source of N source, and the pathway of aspartate utilization was observed. It was confirmed that it was expanded. As a result, a significant increase in the cysteine influx was observed according to the occurrence of ROS, and an effort to regulate the intracellular NADPH balance was observed through the change of metabolites over time. Finally, it was observed that the oncogenic pathway was significantly reduced in the CT mRNA-treated group compared with all untreated groups or controls with other substrate specificities. This study characterizes changes in intracellular metabolites caused by specific dTTP biosynthesis disturbances.

2022-05-06 | GSE202180 | GEO

Transcriptome analysis for CT mRNA treated MDA-MB-231 cells and negative control cells

Project description:We report the altered metabolite changes by processing CT mRNA in the TNBC cell line, MDA-MB-231. It was confirmed that the treatment of CT mRNA disrupted the synthesis of dTTP during nucleic acid metabolism, increasing the signal related to DNA damage in the cell, and that the energy metabolism and NADPH metabolism in the cell were changed for its recovery. The main energy sources, glucose metabolism and glutamine metabolism, are closely linked to the mitochondrial TCA cycle products. In the CT mRNA treatment group, intracellular nucleic acid depletion was observed to increase glutamine metabolism as a source of N source, and the pathway of aspartate utilization was observed. It was confirmed that it was expanded. As a result, a significant increase in the cysteine influx was observed according to the occurrence of ROS, and an effort to regulate the intracellular NADPH balance was observed through the change of metabolites over time. Finally, it was observed that the oncogenic pathway was significantly reduced in the CT mRNA-treated group compared with all untreated groups or controls with other substrate specificities. This study characterizes changes in intracellular metabolites caused by specific dTTP biosynthesis disturbances.

2022-04-28 | GSE201421 | GEO

Glutamine metabolism controls amphiregulin-facilitated chemoresistance to cisplatin in human chondrosarcoma

Project description:Chondrosarcoma is the second most common type of bone cancer. At present, the most effective clinical course of action is surgical resection. Cisplatin is the chemotherapeutic medication most widely used for the treatment of chondrosarcoma; however, its effectiveness is severely hampered by drug resistance. In the current study, we compared cisplatin-resistant chondrosarcoma SW1353 cells with their parental cells via RNA sequencing. Our analysis revealed that glutamine metabolism is highly activated in resistant cells but glucose metabolism is not. Amphiregulin (AR), a ligand of the epidermal growth factor receptor, enhances glutamine metabolism and supports cisplatin resistance in human chondrosarcoma by promoting NADPH production and inhibiting ROS accumulation. The MEK, ERK, and NrF2 signaling pathways were shown to regulate AR-mediated SLC1A5 and GLS expression as well as glutamine metabolism in cisplatin-resistant chondrosarcoma. The knockdown of AR expression in cisplatin-resistant chondrosarcoma cells was shown to reduce the expression of SLC1A5 and GLS in vivo. These results indicate that AR and glutamine metabolism are worth pursuing as therapeutic targets in dealing with cisplatin-resistant human chondrosarcoma.

2023-08-07 | GSE239911 | GEO

Profiling whole-tissue metabolic reprogramming during cutaneous poxvirus infection and clearance

Project description:Background Vaccinia virus (VACV) infection induces prominent changes in host cell metabolism. Little is known about the global metabolic reprogramming that takes place in the whole tissue during viral infection. Here, we performed an unbiased longitudinal metabolomics study in VACV-infected mice to investigate metabolic changes in the tissue during infection. We assessed metabolites in homogenized skin over time in the presence or absence of antigen-specific T cells using untargeted mass spectrometry. VACV infection induced several significant metabolic changes, including in the levels of nucleic acid metabolites (reflecting the impact of viral replication on the skin metabolome). Furthermore, monocyte- and antiviral T cell-produced metabolites, including itaconic acid, glutamine, and glutathione, were significantly increased following infection, highlighting the immune response’s contribution to the global skin metabolome. Additional RNA-Seq of infected skin tissue recapitulated transcriptional changes identified via metabolomics. Overall, our study reveals the metabolic balance of viral replication and the antiviral immune response in the skin and identifies metabolic pathways that could contribute to cutaneous poxvirus control in vivo.

2023-11-09 | GSE236603 | GEO

Bone marrow derived macrophage vs peritoneal macrophage

Project description:Immunometabolism is a rapidly growing field, which has led to greater understanding of innate immune cell functions. Macrophages are at the core of this research: polarized subsets of in vitro-derived cells reportedly utilize select metabolic pathways to maintain their phenotype. However, relevance of these in vitro studies to the in vivo setting is not known, and metabolic requirements are likely dependent on unique physiological and cellular metabolic environments. Here we define the metabolic requirements of peritoneal tissue-resident macrophages, the accessibility of these metabolites to cells in the peritoneum, and we dissect the role of this unique environment in maintaining a crucial macrophage function. We find that the peritoneal cavity is enriched in amino acids, most notably glutamate. Peritoneal tissue-resident macrophages have an extraordinarily large mitochondrial capacity compared with other phagocytes; this is primarily fueled by glutaminolysis, which is additionally required to maintain an extensive respiratory burst. Glutaminolysis fuels the electron transport chain, which is enhanced during tissue-resident macrophage respiratory burst via a switch to dependence of mitochondrial complex-II. This is not dependent on the level of NADPH, but requires p47 maintained NADPH-oxidase activity. Therefore, we propose that tissue-resident macrophages exploit their unique metabolic niche by implementing their glutamine-fueled mitochondrial-rich phenotype to sustain respiratory burst to assault pathogens, showing that cell-specific metabolic underpinning is important for function. Importantly, we also find that glutamine is required for the respiratory burst in human monocytes, which highlights that metabolites are not species-specific and can be the link between cellular mechanism in mouse and man.

2017-10-13 | GSE104920 | GEO

Comparison of transcriptional responses to intracellular RNA and DNA between wild-type and RNase L KO cells

Project description:Analysis of the response to intracellular nucleic acid ligands in wild-type versus RNase L KO cells showed that RNase L KO cells demonstrated an enhanced type I interferon to RNA, but not DNA ligands. Previous studies suggest that mRNAs may be a target of RNase L regulation. To investigate the extent that RNase L activation regulates the antiviral response by targeting of mRNAs, we performed microarray analysis comparing wild-type and RNase L KO cells treated with RIG-I ligand or CT DNA for 6 hours.

2018-01-01 | GSE100655 | GEO

Operation of a TCA cycle subnetwork in the mammalian nucleus

Project description:Nucleic acid and histone modifications critically depend on central metabolism for substrates and co-factors. Although a few enzymes related to the formation of these metabolites have been reported in the nucleus, the corresponding metabolic pathways are considered to function elsewhere in the cell. Here we show that a substantial part of the mitochondrial tricarboxylic acid (TCA) cycle, the biosynthetic hub of epigenetic modification factors, is operational also in the nucleus. Using 13C-tracer analysis, we identified activity of glutamine-to-fumarate, citrate-to-succinate, and glutamine-to-aspartate routes in the nuclei of HeLa cells. Proximity labeling mass-spectrometry revealed a spatial vicinity of the involved enzymes with core nuclear proteins, supporting their nuclear location. We further show nuclear localization of aconitase 2 and 2-oxoglutarate dehydrogenase in mouse embryonic stem cells. Together, our results demonstrate operation of an extended metabolic pathway in the nucleus warranting a revision of the canonical view on metabolic compartmentalization and gene expression regulation.

2022-10-13 | PXD022608 | Pride

Operation of a TCA cycle subnetwork in the mammalian nucleus_mass4tox

Project description:Nucleic acid and histone modifications critically depend on central metabolism for substrates and co-factors. Although a few enzymes related to the formation of these required metabolites have been reported in the nucleus, the corresponding metabolic pathways are considered to function elsewhere in the cell. Here we show that a substantial part of the mitochondrial tricarboxylic acid (TCA) cycle, the biosynthetic hub of epigenetic modification factors, is operational also in the nucleus. Using 13C-tracer analysis, we identified activity of glutamine-to-fumarate, citrate-to-succinate, and glutamine-to-aspartate routes in the nuclei of HeLa cells. Proximity labeling mass-spectrometry revealed a spatial vicinity of the involved enzymes with core nuclear proteins, supporting their nuclear location. We further show nuclear localization of aconitase 2 and 2-oxoglutarate dehydrogenase in mouse embryonic stem cells. Together, our results demonstrate operation of an extended metabolic pathway in the nucleus warranting a revision of the canonical view on metabolic compartmentalization and gene expression regulation.

2022-10-14 | PXD032238 | Pride

Induction of a timed metabolic collapse to overcome cancer chemoresistance

Project description:We identified a transient increase in metabolites involved in glutamine metabolism in chemoresistant acute myeloid leukemia (AML) cells. To further investigate this, we evaluated the transcriptome of AML cells from bone marrow of vehicle-treated mice and mice treated with induction chemotherapy (doxorubicin+cytarabine) at 3 days (iCT group) and 10 days (relapse group) after completion of the chemotherapy.

2020-08-05 | GSE139159 | GEO

Operation of a TCA cycle subnetwork in the mammalian nucleus

Project description:Nucleic acid and histone modifications critically depend on central metabolism for substrates and co-factors. Although a few enzymes related to the formation of these required metabolites have been reported in the nucleus, the corresponding metabolic pathways are considered to function elsewhere in the cell. Here we show that a substantial part of the mitochondrial tricarboxylic acid (TCA) cycle, the biosynthetic hub of epigenetic modification factors, is operational also in the nucleus. Using 13C-tracer analysis, we identified activity of glutamine-to-fumarate, citrate-to-succinate, and glutamine-to-aspartate routes in the nuclei of HeLa cells. Proximity labeling mass-spectrometry revealed a spatial vicinity of the involved enzymes with core nuclear proteins, supporting their nuclear location. We further show nuclear localization of aconitase 2 and 2-oxoglutarate dehydrogenase in mouse embryonic stem cells. Together, our results demonstrate operation of an extended metabolic pathway in the nucleus warranting a revision of the canonical view on metabolic compartmentalization and gene expression regulation. This dataset includes the data relating to the use of LOPIT to determine the subcellular localisation of succinylated proteins.

2022-10-14 | PXD032918 | Pride

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