Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide profiling of YCC16 gastric cancer cell line upon silencing of OCT4 or RXRalpha

ABSTRACT: Dysregulation of OCT4 and RXRalpha has been reported in many cancers. Towards understanding the role of OCT4 and RXRalpha mediated transcriptional programs in gastric cancer, OCT4 and RXRalpha were silenced in YCC16 cells using lentiviral knockdown method. The OCT4 and RXRalpha shRNA encoding lenti-viral infected and non-targeting control (NTC) infected YCC16 cells were selected with puromycin. The stable cells were profiled using Human Transcriptome Array 2.0.

ORGANISM(S): Homo sapiens

PROVIDER: GSE130237 | GEO | 2019/10/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Protein profiles following miRNA-23c and -4328 overexpression in prostate cancer cell lines, PC-3 and 22Rv1

Project description:The 22Rv1 and PC-3 cells were transduced with shMIMIC human lentiviral vectors (Horizon Discovery, Cambridge, UK) to stably overexpress miRNA-23c or -4328. The SMARTvector Non-Targeting Control (NTC) was expressed to serve as a negative control. The vectors contained a turbo green fluorescent protein (turboGFP) and a puromycin resistance gene cassette. After transduction, cells were cultured in a medium supplemented with 5 µg/mL puromycin (Takara Bio, Tokyo, Japan) for antibiotic selection. Overexpression was confirmed by monitoring the turboGFP by fluorescence microscopy and by RT-qPCR analysis of miRNA-23c and -4328 levels. Relative protein quantification was performed to compare protein expression in 22Rv1 and PC-3 single cell clones overexpressing miRNA-23c and -4328, compared to corresponding NTC cells. Single cell clones overexpressing either miRNA-23c (n = 3), -4328 (n = 3) or NTC (n = 3) were analyzed in triplicate.

2023-04-24 | PXD041683 | Pride

ZHBTc4 ES cells stably expressing EGFP vs Nr5a2-EGFP or Oct4-EGFP vs Nr5a2-EGFP

Project description:Gene expression profiles of ZHBTc4 ES cells expressing EGFP, Oct4-EGFP, Nr5a2-EGFP under CAG promoter. Monoclonal cell lines selected by Puromycin were used for analysis. Each of the cell lines was cultured in doxycycline containing media for endogenous Oct4 knock-down. Pupose of this experiment is to investigate the possibility that forced expression of Nr5a2 can replace Oct4 function in the self-renewal of ES cells.

2013-11-05 | GSE52034 | GEO

Genome-wide profiling of YCC16 gastric cancer cell line upon silencing of OCT4 or RXRalpha

Project description:Genome-wide profiling of YCC16 gastric cancer cell line upon silencing of OCT4 or RXRalpha

| PRJNA534425 | ENA

ZHBTc4 ES cells stably expressing EGFP vs Nr5a2-EGFP or Oct4-EGFP vs Nr5a2-EGFP

2013-11-05 | E-GEOD-52034 | biostudies-arrayexpress

ChIP Seq of Oct4, Nanog, H3K27me3 in Oct4+/+ and Oct4 +/- mES cells

Project description:ChIP Seq of Oct4, Nanog, H3K27me3 in Oct4+/+ and Oct4 +/- mES cells

| PRJEB1833 | ENA

Expression data with inducible silencing of HDAC9 in human mesenchymal stem cells (hMSCs)

Project description:In order to study the role of the HDAC9 in human mesenchymal stem cell differentiation, gene expression analysis was performed with inducible silencing of HDAC9 in human mesenchymal stem cell purchasing from Cyagen Biosciences (HUXMA-90011, Guangzhou, China). Transcriptomic analysis performed on mRNA of human mesenchymal stem cells transfected with lentiviral knockdown HDAC9 (lenti-HDAC9) particles revealed down and up regulation of transcripts of hMSCs differentiation genes

2021-03-03 | GSE168056 | GEO

Small extracellular vesicles-delivered LSD1 promotes gastric cancer cell stemness

Project description:Although there are plenty of researches about nucleic acid in small extracellular vesicles (sEVs), properties of proteins identified as sEVs’ cargos and the mechanism of their action in recipient cell are poorly understood. Here, we show that lysine specific demethylase 1 (LSD1), the first identified histone demethylase in 2004, existed in the cell cultured medium of gastric cancer cells. Further investigation confirmed the presence of LSD1 in sEVs from gastric cancer cells and gastric cancer patient plasma, which is the first identified histone demethylase in sEVs. By shuttling from donor cells to recipient gastric cancer cells, sEVs-delivered LSD1 promoted the cancer cell stemness by positively regulating the expression of Nanog, OCT4, SOX2 and CD44, and suppressed the oxaliplatin response of the recipient cells in vitro and in vivo, while LSD1 depleted sEVs failed to suppress the oxaliplatin response. Collectively, our findings give an evidence for LSD1 as a sEVs protein to promote stemness and suppress oxaliplatin response for the first time and constitute a future avenue to predict oxaliplatin response in gastric cancer clinically.

2021-12-22 | PXD020223 | Pride

Small extracellular vesicles-delivered LSD1 promotes gastric cancer cell stemness

2021-07-30 | PXD021511 | Pride

Expression data from human ovarian cancer cell line

Project description:LASS2 was used to identified as a novel suppressor in cancer development and progression. We explored roles of LASS2 in ovarian cancer invasion and metastasis. Lenti-LASS2 and Lenti-vector cells were constructed in 3AO cells through a lentiviral vector system. We preformed global gene expression analysis between Lenti-LASS2 and Lenti-vector cells in accordance with standard Aglient protocols to explore differentially expressed genes and signaling pathways involved by LASS2 overexpression.

2018-07-04 | GSE116562 | GEO

A balanced Oct4 protein interaction network is crucial for maintaining pluripotency

Project description:Oct4 is considered a master transcription factor for pluripotent cell self-renewal and embryo development. It primarily collaborates with other transcriptional factors or coregulators to maintain pluripotency. However, it is still unclear how Oct4 interacts with its partners. Here, we show that the Oct4 linker interface mediates competing and balanced Oct4 protein interactions which are crucial for maintaining pluripotency. Linker mutant ESCs maintain the key pluripotency genes expression, but show decreased expression of self-renewal genes and increased expression of differentiation genes which result in impaired ESCs self-renewal and early embryonic lethality. Linker mutation dose not affect Oct4 genomic binding and transactivation potential, but breaks the balanced Oct4 interactome. In mutant ESCs, the interaction between Oct4 and Klf5 was decreased, but interactions between Oct4 and Cbx1, Ctr9, Cdc73 were increased which disrupt the epigenetic state of ESCs. Overexpression of Klf5 or knockdown Cbx1, Cdc73 rescue the cellular phenotype of linker mutant ESCs by rebalancing Oct4 interactome indicating that different partners interact with Oct4 competitively. Thus, by showing how Oct4 interacts with different partners, we provide novel molecular insights to explain how Oct4 contributes to the maintenance of pluripotency.

2021-12-10 | PXD017456 | Pride

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