Effect of formate on LN229 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE196706 | GEO | 2023/02/06
REPOSITORIES: GEO
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Project description:Effect of formate on LN229 cells
| PRJNA806943 | ENA
Project description:The mitochondrial serine catabolism to formate induces a metabolic switch to a hypermetabolic state with high rates of glycolysis, purine synthesis and pyrimidine synthesis. While formate is a purine precursor it is not obvious link between formate and pyrimidine synthesis. Methods Here we combine phospho-proteome and metabolic profiling to determine how formate induces pyrimidine synthesis. We discover that formate induces CAD phosphorylation. Mechanistically formate induces mTORC1 activity as quantified by S6K1 phosphorylation, which is known to phosphorylate CAD and increase its enzymatic activity. Treatment with the allosteric mTORC1 inhibitor rapamycin abrogates CAD phosphorylation and pyrimidine synthesis induced by formate. We conclude that formate activates mTORC1 and induces pyrimidine synthesis via increasing CAD activity.
2020-09-28 | PXD019347 | Pride
Project description:The invasive nature of glioblastoma (GBM) represents a major clinical challenge contributing to poor outcomes. Invasion of GBM into healthy tissue restricts therapeutic access and surgical resection. Therefore, effective anti-invasive strategies of GBM cells can be key to increase the efficacy of chemotherapy against this devastating disease. As cancer stem or initiating cells are considered to retain the tumorigenic potential in a number of tumors including glioblastoma, we studied the invasion capabilities of glioblastoma initiating cells (GICs) that were isolated from the peritumoral (PT) tissue, which surrounds the tumor mass (TM) and remains in the brain after tumor removal. We found that PT-GICs are less proliferative but more invasive compared to TM-GICs. Gene expression arrays of cells derived from the tumor mass and the peritumoral tissue of three glioblastoma cases
2015-05-13 | E-GEOD-37985 | biostudies-arrayexpress
Project description:Hydrogenotrophic methanogenic Archaea are defined by a H2 requirement for growth. Despite this requirement, many hydrogenotrophs are also capable of growth with formate as an electron donor for methanogenesis. Hydrogenotrophs respond to H2 starvation both phenotypically and at the level of gene expression; however, the responses during growth on formate have not been characterized. Here we report that during continuous culture of Methanococcus maripaludis under defined nutrient conditions, growth yields relative to methane production decreased markedly with either H2 excess or formate excess, suggesting that energy spilling occurs. Using microarray analysis, we show that the expression of genes encoding F420-dependent steps of methanogenesis, including one of two formate dehydrogenases, increased with H2 starvation, but with formate occurred at high levels regardless of limitation or excess. One gene, encoding H2-dependent methylene-tetrahydromethanopterin dehydrogenase, decreased in expression with either H2 limitation or formate limitation. Expression of genes for the second formate dehydrogenase, molybdenum-dependent formylmethanofuran dehydrogenase, and molybdenum transport increased specifically with formate limitation. Of the two formate dehydrogenases, only the first could support growth on formate in batch culture where formate was in excess.
2013-05-03 | GSE42111 | GEO
Project description:Glutamine is an important nutriment for cancer cell growth that provides biological sources for nucleic acid and fatty acid synthesis, but the role of glutaminolysis in signal transduction and glioblastoma (GBM) progression remains little known. Here, we investigated whether GDH1, a key glutamate dehydrogenase, affects the expression levels of signal transduction factors by mRNA expression profiling of wild-type and GDH1 knockdown cells of the glioblastoma cell line LN229 cells
2024-06-30 | GSE268158 | GEO
Project description:In this work, we investigated intracellular pH homeostasis within the thermoacidophilc methanotroph Methylacidiphilum sp. RTK17.1. Our findings show the proton motive force for this species is primarily generated by a pH gradient across the cellular membrane. In batch experiments, the addition of formate resulted in no observable cell growth and, correspondingly, acidification of the cytosol, decreased formate dehydrogenase activity and (presumably) cell-death. Nevertheless, we were able to demonstrable growth on formate as the sole source of metabolizable energy was possible in steady-state (continuous) cultures following the transition from methanol to formate. Under these conditions, biomass productivity yields on formate were 63% less than for growth on methanol. Transcriptome analysis revealed key genes associated with pH homeostasis, methane, methanol and formate metabolism were significantly regulated in response to growth on formate. Collectively, these results suggest environmental formate represents a utilisable source of energy/carbon to the acidophilic methanotrophs during periods of methane starvations and highlights potential short-comings of traditional batch-culture physiological characterisation studies in acidophilic species.
2020-10-31 | GSE145277 | GEO
Project description:Glioblastoma multiforme (GBM) is the most common and aggressive malignant brain tumor among adults, which is characterized by high invasion, migration and proliferation abilities. One important process that contributes to the invasiveness of GBM is the epithelial to mesenchymal transition (EMT). EMT is regulated by a set of defined transcription factors which tightly regulate this process, among them is the basic helix-loop-helix family member, TWIST1. Here we show that TWIST1 is methylated on lysine-33 at chromatin by SETD6, a methyltransferase with expression levels correlating with poor survival in GBM patients. RNA-seq analysis in U251 GBM cells suggested that both SETD6 and TWIST1 regulate cell adhesion and migration processes. We further show that TWIST1 methylation attenuates the expression of the long-non-coding RNA, LINC-PINT, thereby suppressing EMT in GBM. Mechanistically, TWIST1 methylation represses the transcription of LINC-PINT by increasing the occupancy of EZH2 and the catalysis of the repressive H3K27me3 mark at the LINC-PINT locus. Under un-methylated conditions, TWIST1 dissociates from the LINC-PINT locus, allowing the expression of LINC-PINT which leads to increased cell adhesion and decreased cell migration. Together, our findings unravel a new mechanistic dimension for selective expression of LINC-PINT mediated by TWIST1 methylation.
2022-08-12 | PXD029361 | Pride
Project description:The invasive nature of glioblastoma (GBM) represents a major clinical challenge contributing to poor outcomes. Invasion of GBM into healthy tissue restricts therapeutic access and surgical resection. Therefore, effective anti-invasive strategies of GBM cells can be key to increase the efficacy of chemotherapy against this devastating disease. As cancer stem or initiating cells are considered to retain the tumorigenic potential in a number of tumors including glioblastoma, we studied the invasion capabilities of glioblastoma initiating cells (GICs) that were isolated from the peritumoral (PT) tissue, which surrounds the tumor mass (TM) and remains in the brain after tumor removal. We found that PT-GICs are less proliferative but more invasive compared to TM-GICs.
2015-05-13 | GSE37985 | GEO
Project description:The infiltrative nature of Glioblastoma (GBM), the most aggressive primary brain tumor, critically prevents complete surgical resection and masks tumor cells behind the blood brain barrier reducing the efficacy of systemic treatment. New insight in molecular pathways underlying invasion to identify novel invasion-specific molecular targets are likely to improve treatment success and patient outcome. In the present study, we used a genome-wide interference screen to determine invasion-essential genes and identified the AN1/A20 zing finger domain containing protein 3 (ZFAND3) as a crucial driver of invasion in GBM. Using patient-derived cellular GBM models, we validated that loss of ZFAND3 dampens the invasive capacity of GBM, whereas ZFAND3 overexpression increases motility in GBM cells that were initially not invasive. At the mechanistic level, we demonstrate that ZFAND3 activity requires nuclear localization and integral zinc-finger domains. Using integrated transcriptomic and proteomic approaches coupled with reporter assays, we identify ZFAND3 as a novel functional member of a protein complex encompassing PUF60 to activate transcription and GBM cell invasion. Our findings indicate that ZFAND3 regulates the promoter of invasion-related genes such as COL6, FN1 and NRCAM through direct binding to GC rich regions. To harness the therapeutic potential of this transcriptional complex, further investigation in ZFAND3 function in GBM and related invasive cancer types is warranted.
2020-10-08 | MSV000086247 | MassIVE
Project description:Glioblastoma ( GBM) is an astrocytic brain tumor with median survival times of < 15 months, primarily as a result of high infiltrative potential and development of resistance to therapy (i.e., surgical resection, chemoradiotherapy). A prominent feature of the GBM microenvironment is compressive solid stress (CSS) caused by uninhibited tumor growth within the confined skull. We used microarrays to explore the gene expression of LN229 cells treated with 23 Pa CSS as compared to no CSS. The purpose is to detect the up-regulated genes induced by CSS.
2019-12-31 | GSE137210 | GEO