Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ANTICANCER AGENT P-bi-TAT LINKS THE THYROID HORMONE RECEPTOR ON INTEGRIN αvβ3 TO CANCER CELL METABOLISM/ATP GENERATION II

ABSTRACT: Microarray analysis was carried out on human GBM cells exposed to P-bi-TAT (10-6 M tetrac equivalent) for 24 h. P-bi-TAT significantly downregulated electron transport chain genes ATP5A1 (ATP synthase A1), ATP51, ATP5G2, COX6B1 (cytochrome c oxidase subunit 6B1), NDUFA8 (NADH dehydrogenase [ubiquinone] FA8), NDUFV2 and other NDUF genes, SLC25A6 (solute carrier group 2), UCP2 ([mitochondrial] uncoupling protein 2) and COX5A. The NDUF and ATP genes are also relevant to control of oxidative phosphorylation and transcription. Six additional NDUF genes linked to oxidative phosphorylation were affected. Conclusions. P-bi-TAT caused downregulation of expression of a panel of genes involved in electron transport, oxidative phosphorylation, and cytoplasmic ribosomal protein generation in GBM cells. A key component of the anticancer activity of P-bi-TAT relates to disordering of ATP generation mechanisms in tumor cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE140449 | GEO | 2020/08/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ANTICANCER AGENT P-bi-TAT LINKS THE THYROID HORMONE RECEPTOR ON INTEGRIN αvβ3 TO CANCER CELL METABOLISM/ATP GENERATION.

Project description:Microarray analysis was carried out on human GBM primary cells (GBM 10181360) and GBM cell line (U87) exposed to P-bi-TAT (10-6 M tetrac equivalent) for 24 h and 48 h. P-bi-TAT significantly downregulated electron transport chain genes ATP5A1 (ATP synthase A1), ATP51, ATP5G2, COX6B1 (cytochrome c oxidase subunit 6B1), NDUFA8 (NADH dehydrogenase [ubiquinone] FA8), NDUFV2 and other NDUF genes, SLC25A6 (solute carrier group 2), UCP2 ([mitochondrial] uncoupling protein 2) and COX5A. The NDUF and ATP genes are also relevant to control of oxidative phosphorylation and transcription. Six additional NDUF genes linked to oxidative phosphorylation were affected. Conclusions. P-bi-TAT caused downregulation of expression of a panel of genes involved in electron transport, oxidative phosphorylation, and cytoplasmic ribosomal protein generation in GBM cells. A key component of the anticancer activity of P-bi-TAT relates to disordering of ATP generation mechanisms in tumor cells

2021-09-11 | GSE183776 | GEO

ANTICANCER AGENT P-bi-TAT LINKS THE THYROID HORMONE RECEPTOR ON INTEGRIN αvβ3 TO CANCER CELL METABOLISM/ATP GENERATION

Project description:Microarray analysis was carried out on human GBM cells exposed to P-bi-TAT (10-6 M tetrac equivalent) for 24 h. P-bi-TAT significantly downregulated electron transport chain genes ATP5A1 (ATP synthase A1), ATP51, ATP5G2, COX6B1 (cytochrome c oxidase subunit 6B1), NDUFA8 (NADH dehydrogenase [ubiquinone] FA8), NDUFV2 and other NDUF genes, SLC25A6 (solute carrier group 2), UCP2 ([mitochondrial] uncoupling protein 2) and COX5A. The NDUF and ATP genes are also relevant to control of oxidative phosphorylation and transcription. Six additional NDUF genes linked to oxidative phosphorylation were affected. Conclusions. P-bi-TAT caused downregulation of expression of a panel of genes involved in electron transport, oxidative phosphorylation, and cytoplasmic ribosomal protein generation in GBM cells. A key component of the anticancer activity of P-bi-TAT relates to disordering of ATP generation mechanisms in tumor cells.

2020-08-28 | GSE140272 | GEO

Anticancer Agent P-Bi-Tat Links The Thyroid Hormone Receptor On Integrin Αvβ3 To Cancer Cell Metabolism/Atp Generation [Suit2-P-biTAT]

Project description:Microarray analysis was carried out on human SUIT2 cells exposed to P-bi-TAT (10-6 M tetrac equivalent) for 24 h. P-bi-TAT significantly downregulated electron transport chain genes ATP5A1 (ATP synthase A1), ATP51, ATP5G2, COX6B1 (cytochrome c oxidase subunit 6B1), NDUFA8 (NADH dehydrogenase [ubiquinone] FA8), NDUFV2 and other NDUF genes, SLC25A6 (solute carrier group 2), UCP2 ([mitochondrial] uncoupling protein 2) and COX5A. The NDUF and ATP genes are also relevant to control of oxidative phosphorylation and transcription. Six additional NDUF genes linked to oxidative phosphorylation were affected. Conclusions. P-bi-TAT caused downregulation of expression of a panel of genes involved in electron transport, oxidative phosphorylation, and cytoplasmic ribosomal protein generation in GBM cells. A key component of the anticancer activity of P-bi-TAT relates to disordering of ATP generation mechanisms in tumor cells.

2022-04-27 | GSE180896 | GEO

Anticancer Agent Fb-Pmt Links The Thyroid Hormone Receptor On Integrin Αvβ3 To Cancer Cell Metabolism/Atp Generation [MOH-fbPMT]

Project description:Microarray analysis was carried out on human MOH cells exposed to fb-PMT (10e-6 M tetrac equivalent) for 24 h. fb-PMT significantly downregulated electron transport chain genes ATP5A1 (ATP synthase A1), ATP51, ATP5G2, COX6B1 (cytochrome c oxidase subunit 6B1), NDUFA8 (NADH dehydrogenase [ubiquinone] FA8), NDUFV2 and other NDUF genes, SLC25A6 (solute carrier group 2), UCP2 ([mitochondrial] uncoupling protein 2) and COX5A. The NDUF and ATP genes are also relevant to control of oxidative phosphorylation and transcription. Six additional NDUF genes linked to oxidative phosphorylation were affected. Conclusions. fb-PMT caused downregulation of expression of a panel of genes involved in electron transport, oxidative phosphorylation, and cytoplasmic ribosomal protein generation in MOH cells. A key component of the anticancer activity of fb-PMT relates to disordering of ATP generation mechanisms in tumor cells.

2022-07-01 | GSE180889 | GEO

Anticancer Agent Fb-Pmt Links The Thyroid Hormone Receptor On Integrin Αvβ3 To Cancer Cell Metabolism/Atp Generation [Suit2-fbPMT]

Project description:Microarray analysis was carried out on human SUIT2 cells, cells exposed to fb-PMT (10-6 M tetrac equivalent) for 24 h. fb-PMT significantly downregulated electron transport chain genes ATP5A1 (ATP synthase A1), ATP51, ATP5G2, COX6B1 (cytochrome c oxidase subunit 6B1), NDUFA8 (NADH dehydrogenase [ubiquinone] FA8), NDUFV2 and other NDUF genes, SLC25A6 (solute carrier group 2), UCP2 ([mitochondrial] uncoupling protein 2) and COX5A. The NDUF and ATP genes are also relevant to control of oxidative phosphorylation and transcription. Six additional NDUF genes linked to oxidative phosphorylation were affected. Conclusions. fb-PMT caused downregulation of expression of a panel of genes involved in electron transport, oxidative phosphorylation, and cytoplasmic ribosomal protein generation in SUIT2 cells, cells. A key component of the anticancer activity of fb-PMT relates to disordering of ATP generation mechanisms in tumor cells.

2022-07-01 | GSE180895 | GEO

Gene expression during CCK-induced damaged pancreatic acinar cells with or without the addition of OCA

Project description:Obeticholic acid (OCA) has shown pharmacological protection activity in acinar cell injury and pancreatic necrosis in vitro. RNA sequencing was performed by extracting mRNA from CCK-induced damaged pancreatic acinar cells with or without the addition of OCA. Gene enrichment analysis by Kyoto Encyclopedia of Genes and Genomes (KEGG) identified oxidative phosphorylation in the top ten significantly changed pathways. Similarly, Gene Set Enrichment Analysis (GSEA) enrichment analysis revealed clear alterations in "mitochondrial ATP synthesis coupled electron transport", "mitochondrial respiratory chain complex assembly", "NADH dehydrogenase complex assembly", and "oxidative phosphorylation".

2023-12-31 | GSE245795 | GEO

DIA-MS proteomics of untreated and TAT-Cx43266-283-treated G166 GSCs

Project description:Glioblastoma (GBM) is the most frequent and aggressive primary brain cancer. Our studies have shown that the Src inhibitor, TAT-Cx43266-283, exerts antitumor effects in different preclinical models of GBM, including fresh specimens from GBM patients, and enhances survival in glioma-bearing mice. Because addressing TAT-Cx43266-283 mechanism of action is essential to translate these results to a clinical setting, in this study we carried out an unbiased proteomic approach in human glioblastoma stem cells (GSCs). Data-independent acquisition mass spectrometry proteomics allowed the identification and quantification of 6,561 proteins, of which 190 were modified by TAT-Cx43266-283. Our results are consistent with the inhibition of Src as the mechanism of action of TAT-Cx43266-283 and unveils additional crucial proteins. Altogether, this study expands the knowledge about the mechanism of action of TAT-Cx43266-283, providing a rationale for therapy combination and supporting its use in GBM clinical trials.

2024-06-22 | PXD045883 | Pride

Tumor-Associated Microglia Secrete Extracellular ATP to Support Glioblastoma Progression

Project description:Glioblastoma (GBM) is a highly aggressive brain tumor with poor prognosis and high recurrence rates. The complex immune microenvironment of GBM is highly infiltrated by tumor-associated microglia and macrophages (TAMs). TAMs are known to be heterogeneous in their functional and metabolic states and can transmit either pro-tumoral or anti-tumoral signals to glioma cells. Here, we performed bulk RNA-seq and single-cell RNA-seq on GBM patient samples, which revealed increased ATP synthase expression and oxidative phosphorylation (OXPHOS) activity in TAMs located in the tumor core relative to the tumor periphery. Both in vitro and in vivo models displayed similar trends of augmented TAM mitochondrial activity, along with elevated mitochondrial fission, glucose uptake, mitochondrial membrane potential, and extracellular ATP (eATP) production by TAMs in the presence of GBM cells. Tumor-secreted factors, including GM-CSF, induced the increase in TAM eATP production. Elevated eATP in the GBM microenvironment promoted glioma growth and invasion by activating the P2X purinoceptor 7 (P2X7R) on glioma cells. Inhibition of the eATP-P2X7R axis attenuated tumor cell viability in vitro and reduced tumor size and prolonged survival in glioma-bearing mouse models. Overall, this study revealed elevated TAM-derived eATP in GBM and provided the basis for targeting the eATP-P2X7R signaling axis as a therapeutic strategy in GBM.

2024-08-30 | GSE275293 | GEO

Anti-Warburg effect elicited by mitochondrial biogenesis drives differentiation of glioblastoma cells into astroglial cells

Project description:Glioblastoma (GBM) is among the most aggressive of human cancers. Although differentiation therapy has been proposed to be potential approach to treat GBM, the mechanisms of induced differentiation remain poorly defined. Here, we established the induced differentiation model of GBM by using cAMP activators, which specifically directed GBM into astroglia. Next, transcriptomic and proteomic analyses uncovered oxidative phosphorylation and mitochondrial biogenesis were involved in induced differentiation of GBM. Further investigation showed dbcAMP reversed Warburg effect evidenced by increase of oxygen consumption and reduction of lactate production. Stimulated mitochondrial biogenesis downstream of CREB/PGC1α pathway triggered metabolic shift and differentiation. Blocking mitochondrial biogenesis by mdivi1 or silencing PGC1α abrogated differentiation, reversely over-expression of PGC1α elicited differentiation. In GBM xenograft models and patient-derived GBM samples, cAMP activators also induced tumor growth inhibition and differentiation. This study shows mitochondrial biogenesis and metabolic switch to oxidative phosphorylation drive the differentiation process of tumor cells.

2017-11-10 | GSE89745 | GEO

Selective Inhibitors of mTORC1 Activate 4EBP1 and Suppress Tumor Growth

Project description:The clinical benefit of current mTOR inhibitors is limited, perhaps reflecting their intrinsic pharmacological profiles. Rapamycin analogs selectively inhibit mTORC1, but fail to suppress phosphorylation of the mTORC1 substrate 4EBP1, a translational repressor that is a key driver of oncogenic mTORC1 signaling. mTOR kinase active-site inhibitors fully suppress mTORC1 and phosphorylation of its substrates, but are active against mTORC2 and additional kinases, potentially contributing to tolerability limitations. The prototype bi-steric inhibitor RapaLink-1 exploits the selective mTORC1 interactions of rapamycin and the broad mTOR kinase inhibitory effects of an active-site inhibitor, through covalent linkage of the two pharmacophores to achieve complete mTORC1/2 inhibition. We demonstrate that the anti-proliferative activity of RapaLink-1 is dependent upon mTORC1 and suppression of 4EBP1 phosphorylation. Using a rational design strategy, we tuned the affinities of the rapamycin core and ATP-mimetic moieties to create novel bi-steric inhibitors with enhanced mTORC1 selectivity and potency against 4EBP1 phosphorylation. mTORC1-selective bi-steric compounds produced durable inhibition of 4EBP1 phosphorylation in vitro and in vivo, and drove tumor regressions at well-tolerated doses in xenograft models of breast cancer.

2021-04-05 | GSE138417 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data