Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of differentially expressed miRNAs after knockdown of ELF3-AS1 in gastric cancer

ABSTRACT: In this study, we used miRNA sequencing to analyze and identify possible miRNAs that can be regulated by and ELF3-AS1 in gastric cancer. The results showed that lncRNA ELF3-AS1 knockdown decreased the expression of miR-33a/b and miR-203a. Due to miR-33a/b and miR-203a were able to target SNAI2 expression, and ELF3-AS1 knockdown significantly upregulates SNAI2 expression, we speculated ELF3-AS1 may negatively regulate SNAI2 expression through positively regulating the expression of miR-33a/b and miR-203a in GC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE161553 | GEO | 2021/10/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Knockdown of lncRNA ELF3-AS1 in two gastric cancer cell lines

Project description:Our data showed that ELF3-AS1 was a nuclear lncRNA, and its biofunction in cancers is largely unknown to date. To explore the function of lncRNA ELF3-AS1 in gastric cancer, loss-of-function study was performed in SGC7901 and AGS cell lines. RNA sequencing studies showed that the expression of almost all the histone coding genes were significantly increased after knocking down of ELF3-AS1 in SGC7901 and AGS cell lines.

2021-10-01 | GSE161291 | GEO

Knockdown of lncRNA ELF3-AS1 in two gastric cancer cell lines

Project description:Knockdown of lncRNA ELF3-AS1 in two gastric cancer cell lines

| PRJNA676142 | ENA

Knockdown of ILF2/ILF3 (NF45/NF90) in the gastric cancer cell line SGC7901

Project description:Our data showed that lncRNA ELF3-AS1 could bind on the exon1 of ELF3-201 to form a double-stranded RNA molecule. This double-stranded RNA could interact with ILF2/ILF3 complex. To explore the biofunction of the interaction between ELF3-AS1 and ILF2/ILF3 complex, loss-of-function studies regarding ILF2 and ILF3 were performed in SGC7901 cell line. RNA sequencing studies showed that knockdown of ILF3 significantly decreased ELF3-AS1, while knockdown of ILF2 significantly increased ELF3-AS1 and NF90 expression. Our data revealed that ILF2/ILF3 complex interacted with ELF3-AS1/ELF3 double-stranded RNA and regulated their transcripts stability.

2021-10-01 | GSE161544 | GEO

Identification of differentially expressed miRNAs after knockdown of ELF3-AS1 in gastric cancer

Project description:Identification of differentially expressed miRNAs after knockdown of ELF3-AS1 in gastric cancer

| PRJNA678706 | ENA

Expression profiling analysis of ELF3-knockdown (KD) and control human bile duct cells

Project description:An immortalized normal epithelial cell line of common bile duct origin (HBDEC2 cells) was established. An ELF3 gene knockdown clone was obtained using microRNA-155-based conditional RNA interference targeting the human ELF3 gene (5′-AGGTTCTGCTGGATCAGCT-3′) and EGFPmiR, targeting EGFP as a control (EGFP-miR; 5′-ACAAGCTGGTACAACTACA-3′).

2020-08-27 | GSE148106 | GEO

Gene expression profiling in prostate cancer cell lines transfected with miR-33a

Project description:In this study, we aimed to investigate the functional roles of miR-33a in PCa.We investigated the relative miR-33a level in normal and tumor prostate samples as well as PCa cell lines. Then, we performed a detailed functional analysis of mir-33a in LNCaP and VCaP PCa cells and evaluated proliferative, invasive and anchorage independent growth potential of cells upon overexpression and knockdown of miR-33a. We next explored the potential direct targets of miR-33a in PCa cells via utilizing gene expression microarray analysis, bioinformatics search, further qRT-PCR, western blot, and luciferase assay confirmation. Our results demonstrated that miR-33a is significantly downregulated in PCa tumor samples and PCa cell lines, pointing its tumor suppressor potential in PCa. Overexpression and knockdown of miR-33a significantly altered the proliferative, invasive and anchorage independent growth potentials of cells through altering the expression of its direct target PIM1. Ectopic induction of MiR-33a expression reversed the impacts of PIM1 overexpression on cellular phenotypes associated with PCa progression. Our results suggest that mir-33a exerts its tumor suppressor potential through targeting its direct target PIM1 and carries crucial roles in PCa tumorigenesis.

2017-10-31 | GSE89034 | GEO

SBF2-AS1 promotes tumorigenesis as a miRNA sponge in lung cancer

Project description:Long noncoding RNA (lncRNA) play important roles in the pathogenesis of cancer. LncRNA SBF2-AS1is unregulated in lung cancer tissues, while its biological function and molecular mechanism are largely unknown. RNA sequencing results suggest cell cycle-related genes are altered after SBF2-AS1 knockdown. In vivo and in vitro experiments confirm SBF2-AS1 could promote tumorigenesis of lung cancer. Further experiments prove SBF2-AS1 could bind with miR-338-3p and miR-362-3p to regulate various cell cycle-related genes, including E2F1. These results indicate the existence of ceRNA network driven by SBF2-AS1 through sponging miRNAs.

2017-08-24 | GSE103016 | GEO

Long Noncoding RNA HNF1A-AS1 Regulates Proliferation and Migration in Esophageal Adenocarcinoma Cells

Project description:Objectives: Long non-coding RNAs (lncRNAs) have been shown to play important roles in the development and progression of cancer. However, functional lncRNAs and their downstream mechanisms are largely unknown in the molecular pathogenesis of esophageal adenocarcinoma (EAC) and its progression. Design: lncRNAs that are abnormally upregulated in EACs were identified by RNA-seq analysis, followed by quantitative RT-PCR (qRTPCR) validation using tissues from 31 EAC patients. Cell biological assays in combination with siRNA-mediated knockdown were performed in order to probe the functional relevance of these lncRNAs. Results: We discovered that a lncRNA, HNF1A-AS1, is markedly upregulated in human primary EACs relative to their corresponding normal esophageal tissues (mean fold change 7.2, p<0.01). We further discovered that HNF1A-AS1 knockdown significantly inhibited cell proliferation and anchorage independent growth, suppressed S-phase entry, and inhibited cell migration and invasion in multiple in vitro EAC models (p<0.05). A gene ontological analysis revealed that HNF1A-AS1 knockdown preferentially affected genes that are linked to assembly of chromatin and the nucleosome, a mechanism essential to cell cycle progression. The well-known cancer-related lncRNA, H19, was the gene most markedly inhibited by HNF1A-AS1 knockdown. Consistent to this finding, there was a significant positive correlation between HNF1A-AS1 and H19 expression in primary EACs (p<0.01). In order to identify novel oncogenic lncRNAs in esophageal adenocarcinogenesis, we carried out RNA-seq of a matched NE-BE-EAC tissue pair

2013-10-21 | E-GEOD-48240 | biostudies-arrayexpress

Knockdown of lncRNA NR2F1-AS1 in gastric cancer cells

Project description:Our data showed that NR2F1-AS1 functions oncogenic roles in gastric cancer (GC), but the underlying molecular mechanism remains largely unknown to date. To explore the function of lncRNA NR2F1-AS1 in gastric cancer, loss-of-function and RNA sequencing studies were performed in SGC7901 cell line. The results showed that depletion of NR2F1-AS1 significantly decreased the expression of VAMP7. Interestingly, VAMP7 was also a target gene of miR-29a-3p. Our data showed that NR2F1-AS1 promotes GC progression through regulating miR-29a/VAMP7 axis.

2021-10-07 | GSE183538 | GEO

Expression profiling analysis of an inducible ELF3-expressing and control human bile duct cells [inducible ELF3]

Project description:An immortalized normal epithelial cell line of common bile duct origin (HBDEC2 cells) was established. An inducible ELF3-expressing was generated by infection with the retrovial vector pRetroX-TetOne-Puro-ELF3-flag, expressing ELF3 fused to a flag-tag.

2020-08-27 | GSE148107 | 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