Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Knockdown of Akt1/2 by CRISPR/Cas9 suppresses the metastasis of human prostate cancer cells CWR22rv1 in vitro and in vivo

ABSTRACT: Knockdown of Akt1/2 by CRISPR/Cas9 suppresses the metastasis of human prostate cancer cells CWR22rv1 in vitro and in vivo

PROVIDER: PRJNA682832 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13204914_1.fastq.gz	Fastqsanger.gz
	SRR13204914_2.fastq.gz	Fastqsanger.gz
	SRR13204915_1.fastq.gz	Fastqsanger.gz
	SRR13204915_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Knockdown of Akt1/2 by CRISPR/Cas9 suppresses the metastasis of human prostate cancer cells CWR22rv1 in vitro and in vivo

Project description:Our findings will initially map out the downstream signal pathways of Akt and AR mutual feedback to regulate CaP metastasis through the study of these scientific assumptions, which will provide targets for the development of new precise treatments for prostate cancer.

2021-02-17 | GSE162743 | GEO

PRSS8 Suppresses Colorectal Carcinogenesis and Metastasis.

Project description:PRSS8 Suppresses Colorectal Carcinogenesis and Metastasis.

| PRJNA475479 | ENA

miRNA arrays for LPS-activated Akt1+/+ and Akt1-/- macrophages

Project description:MicroRNAs regulated by lipopolysaccharide (LPS) target genes that contribute to the inflammatory phenotype. Here we showed that the protein kinase Akt1, which is activated by LPS, positively regulated miRNAs let-7e, miR-181c but negatively regulated miR-155 and miR-125b. In silico analyses and transfection studies revealed that let-7e repressed Toll-like receptor 4 (TLR4) whereas miR-155 repressed SOCS1, two proteins critical for LPS-driven TLR signalling, which regulate endotoxin sensitivity and tolerance. As a result, Akt1-/- macrophages exhibited increased responsiveness to LPS in culture and Akt1-/- mice did not develop endotoxin tolerance in vivo. Overexpression of let-7e and suppression of miR-155 in Akt1-/- macrophages restored sensitivity and tolerance to LPS in culture and in animals. These results indicate that Akt1 regulates the response of macrophages to LPS by controlling miRNA expression. The data deposited here contain the entire analysis of miRNA profile of Akt1+/+ and Akt1-/- thioglycollate elicited peritoneal macrophages following stimulation with LPS for 3 hours in culture.

2009-08-21 | GSE17421 | GEO

circNFIB suppresses lymphatic metastasis of pancreatic cancer

Project description:circNFIB suppresses lymphatic metastasis of pancreatic cancer

| PRJNA562706 | ENA

CircNCOR1 suppresses lymphatic metastasis in bladder cancer

Project description:CircNCOR1 suppresses lymphatic metastasis in bladder cancer

| PRJNA789492 | ENA

STING suppresses the reactivation of dormant metastasis

Project description:STING suppresses the reactivation of dormant metastasis

| PRJNA868358 | ENA

miRNA arrays for LPS-activated Akt1+/+ and Akt1-/- macrophages

2009-08-21 | E-GEOD-17421 | biostudies-arrayexpress

Impact of AKT1 on cell invasion and radiosensitivity on breast cancer brain metastasis

Project description:Impact of AKT1 on cell invasion and radiosensitivity on breast cancer brain metastasis

| PRJEB55989 | ENA

SETDB1-TRIM28 complex suppresses antitumor immunity [CRISPR/Cas9 screen]

Project description:SETDB1-TRIM28 complex suppresses antitumor immunity [CRISPR/Cas9 screen]

| PRJNA755293 | ENA

BRMS1L suppresses breast cancer metastasis by inducing epigenetic silence of FZD10

Project description:BRMS1L (breast cancer metastasis suppressor 1 likeM-oM-<M-^LBRMS1-like) is a component of the SIN3A-HDAC corepressor complex that suppresses target gene transcription. Here, we show that reduced BRMS1L in breast cancer tissues is associated with tumor metastasis and poor patient survival. Functionally, BRMS1L inhibits migration and invasion of breast cancer cells by inhibiting epithelial-mesenchymal transition (EMT). These effects are mediated by epigenetic silencing of FZD10, a receptor for Wnt signaling, by facilitating the recruitment of HDAC1 to its promoter and enhancing histone H3K9 deacetylation. Consequently, BRMS1L-induced FZD10 silencing inhibits aberrant activation of WNT3-FZD10-M-oM-^AM-"-catenin signaling. Furthermore, BRMS1L is a target of miR-106b and miR-106b upregulation leads to BRMS1L reduction in breast cancer cells. RNAi-mediated silencing of BRMS1L expression promotes metastasis of breast cancer xenografts in immunocompromised mice, while ectopic BRMS1L expression inhibits metastasis. Therefore, BRMS1L provides an epigenetic regulation of Wnt signaling in breast cancer cells and acts as a breast cancer metastasis suppressor. Ther transfection analysis used here were further desxribed in Chang Gong, eta al.2013. miR-106b expression determines the proliferation paradox of TGF-M-NM-2 in breast cancer cells. Oncogene. 2013 A two chip study using total RNA recovered from MDA-MB-231 breast cancer cells transfected with negative control vector or vector overexpressing BRMS1L for 24 hours. Each chip measures the expression 45033 genes were collected from the authoritative data source including NCBI.

2014-09-12 | E-GEOD-61354 | biostudies-arrayexpress

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