Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling of human neuroblastoma cell line SMS-KCNR treated with DMSO, simvastatin at 5 µM or simvastatin at 5 µM plus mevalonate at 2 mM for 30 hours

ABSTRACT: Gene expression profiling of human neuroblastoma cell line SMS-KCNR treated with DMSO, simvastatin at 5 µM or simvastatin at 5 µM plus mevalonate at 2 mM for 30 hours

PROVIDER: PRJNA891335 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiling of human neuroblastoma cell line SMS-KCNR treated with DMSO, simvastatin at 5 µM or simvastatin at 5 µM plus mevalonate at 2 mM for 30 hours

Project description:Microarray gene expression profiling reveals that simvastatin regulates the expression of M phase cell cycle genes and mevalonate metabolism

2023-05-01 | GSE215949 | GEO

Role of mevalonate pathway intermediates in anticancer effect of statins

Project description:Simvastatin has been widely used for treatment of hypercholesterolemia due to its ability to inhibit HMG-CoA reductase, the rate limiting enzyme of de novo cholesterol synthesis via mevalonate pathway. Its inhibitory action causes also depletion of pathway intermediates, farnesyl pyrophosphate (FPP) and geranyl-geranyl pyrophosphate (GGPP), which are inevitable for proper targeting of small GTPases (e.g. Ras proteins) to their site of action. We profiled by array the gene expression of MIA PaCa-2 cells treated with simvastatin, FPP, GGPP and their combinations. The inhibitory effect of statins on GFP-K-Ras protein trafficking were partially prevented by addition of the mevalonate pathway intermediates. We conclude that the anticancer effect of simvastatin is to a large extent mediated through isoprenoid intermediates of the mevalonate pathway.

2018-03-31 | E-MTAB-3263 | biostudies-arrayexpress

Mevalonate pathway inhibition affects bladder cancer metastasis

Project description:Metastasis is an important factor affecting the prognosis and survival of bladder cancer (BLCA) patients. Our previous study found that the mevalonate pathway is associated with the migratory ability of BLCA cells, but the exact mechanism is unclear. Here, we found that BLCA patients with mevalonate pathway activation had a poorer prognosis. Inhibition of the mevalonate pathway (FDPS knockdown, simvastatin or zoledronic acid) significantly reduced the migratory ability of BLCA cells. Therefore, we tested the changes of key genes after knocking down the key enzymes of the mevalonate pathway, FDPS and SQLE1, and the transcription factor YY1 in bladder cancer cells using RNA sequencing.

2024-09-08 | GSE252007 | GEO

Mevalonate pathway inhibition affects bladder cancer metastasis

Project description:Metastasis is an important factor affecting the prognosis and survival of bladder cancer (BLCA) patients. Our previous study found that the mevalonate pathway is associated with the migratory ability of bladder cancer cells, but the exact mechanism is unclear. Here, we found that BLCA patients with mevalonate pathway activation had a poorer prognosis. Inhibition of the mevalonate pathway (simvastatin or zoledronic acid) resulted in a significant decrease in the migratory ability of BLCA cells. Therefore, we used proteomics to detect simvastatin- or zoledronic acid-treated BLCA cells to explore the effect of the mevalonate pathway on key proteins in BLCA cells.

2024-09-09 | PXD048067 |

Induction of resistance to NTRK inhibitors via mevalonate pathway by HMGCS2

Project description:Paretal KM12 and NTRK inhibitor resistant cells established from KM12 in our laboratory was compared to search for and analyze significant factors related to resistance mechanism. To investigated the mechanism of resistance to NTRK-TKI, we establish resistant cells to three type NTRK-TKIs (Larotrectinib, Entrectinib and Selitrectinib) by step -wise methods using KM12 with TPM5-NTRK1 rearrangement for 6 months. (KM12-LR, KM12-ER and KM12-SR) 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2) over expression was observed commonly in three resistance cells. Lower expression of SREBP2 and PPARα in two cells (KM12-ER and KM12-SR) in which HMGCS2 was more overexpressed than parental KM12 and KM12-LR. In resistant cells, knockdown of HMGCS2 using small interfering RNA improved NTRK-TKIs sensitivity, but further treatment with mevalonolactone after knockdown HMGCS2 reintroduced NTRK-TKIs resistance. In addition, simvastatin and silibinin had synergic effect with NTRK-TKIs to resistant cells and delayed tolerance was observed after sustained exposure to clinical concentrations of NTRK-TKI and simvastatin against KM12. These results suggested that HMGCS2 overexpression induces resistance to NTRK-TKI via the mevalonate pathway. In addition, statin inhibited mevalonate pathway may be useful for overcoming this mechanism resistance.

2023-03-10 | GSE225681 | GEO

Investigate the affect of CASZ1b on chromatin accessibility in SMS-CTR cells

Project description:In SMS-CTR cells, the overexpression of CASZ1b in SMS-CTR cells led to a modification of regional chromation accessibility.

2019-12-26 | GSE126140 | GEO

Genome-wide mapping of CASZ1 binding sites in differentiated SMS-CTR cells [Trametinib]

Project description:MEK inhibitor trametinib induces SMS-CTR cell differentiation and up-regulates CASZ1 expression. We identified genome-wide binding sites of CASZ1 in differentiated SMS-CTR cells.

2019-12-26 | GSE126143 | GEO

RNA-sequencing analysis to investigate genes regulated by CASZ1 in SMS-CTR cells

Project description:In this study we identified genes regulated by CASZ1b in SMS-CTR cells

2019-12-26 | GSE126145 | GEO

Genome-wide mapping of CASZ1b binding sites and investigate its effect on chromatin status in SMS-CTR cells [CTRtetCASZ1b]

Project description:In SMS-CTR cells, we identified genomewide binding sites of CASZ1b. The overexpression of CASZ1b in SMS-CTR cells led to a regional epigenetic modification.

2019-12-26 | GSE126142 | GEO

This study examined gene expression in zebrafish embryos exposed to 0 (0.01% DMSO), 16 µM, or 32 µM perfluorobutane sulfonate.

Project description:This study examined gene expression in zebrafish embryos exposed to 0 (0.01% DMSO), 16 µM, or 32 µM perfluorobutane sulfonate.

| PRJNA471075 | ENA

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