Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE180889 | GEO | 2022/07/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

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

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 | GSE140449 | 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 P-bi-TAT LINKS THE THYROID HORMONE RECEPTOR ON INTEGRIN αvβ3 TO CANCER CELL METABOLISM/ATP GENERATION

2020-08-28 | GSE140272 | 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 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

Novel Thyrointegrin αvβ3 antagonist (fp-PMT) with potent affinity in the treatment of cancer

Project description:Microarray analysis was carried out on Glioblastoma (GBM 10181360, GBM 021913 and U87 cells), Bladder cancer (JBV253), skin cancer (A375) and Acute Myelod Leukemia (AML) (KG1A and K562 cells) exposed to fb-PMT at 30 µM concentration. Our genome-wide microarray screens demonstrated that fb-PMT appears to exert its potent anticancer actions on human cancer cells through the molecular interference mechanism with multiple signaling pathways supporting growth and survival of leukemic cells. Notably, fb-PMT had a significant effect on different molecular pathways that contribute to the anticancer activity such as cell cycle control (MYC), survival and maintenance of stem cells (HIF1A; TFAP2C), essential features of the malignant phenotype (TWIST1; SNAI). Furthermore, the fb-PMT-induced significant transcriptional pathway’s activation includes RB1; IRF9; MAML1; RAP1A; and GATA4 pathways, which known to play an important role in anticancer activity. Finally, Consistent with our previous reports on the crosstalk between integrin αvβ3 and ERα which contributes to the induced proliferation of cancer cells, we found that fb-PMT interference with estrogen signaling. The αvβ3 agonist (thyroid hormone) was associated with increased phosphorylation and nuclear enrichment of estrogen receptor α (ERα).

2021-09-11 | GSE183772 | 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

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

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

| PRJNA749946 | ENA

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

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

| PRJNA749957 | ENA

The protozoan inhibitor Atovaquone affects mitochondrial respiration and shows in vitro efficacy against glucocorticoid-resistant cells in childhood B-cell acute lymphoblastic leukaemia

Project description:Atovaquone is a well-tolerated drug used in the clinic mainly against malaria. Being a ubiquinone analogue, this drug inhibits co-enzyme Q10 of the electron transport chain (ETC) affecting oxidative phosphorylation and cell metabolism. In this study we tested the effect of Atovaquone on cALL cells in vitro. The outcome of this inhibition of the ETC is a marked decrease in basal respiration and ATP levels, as well as reduced proliferation, cell cycle arrest and induction of apoptosis. On the transcriptional level, we see changes in cellular metabolic processes, activation of p53 pathway, apoptosis, enrichment of cell cycles genes and downregulation of hypoxia and mTORC1 signalling pathway.

2021-02-26 | GSE161959 | 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