Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

FAM83H-AS1 silencing in MCF7 breast cancer cells

ABSTRACT: We silenced FAM83H-AS1 shRNAs in cell line MCF7 carried a ~75% silencing compared to thenegative control (NC). We evaluated the role of FAM83H-AS1 on oncogenic phenotypes in the MCF7 breast cancer cell line model. The knockdown of FAM83H-AS1 was achieved with ~75% of silencing efficiency. A complete transcriptomic analysis after silencing of FAM83H-AS1 revealed an impact on the global expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE135466 | GEO | 2020/12/12

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

FAM83H-AS1 silencing in MCF7 breast cancer cells

Project description:FAM83H-AS1 silencing in MCF7 breast cancer cells

| PRJNA558978 | ENA

Effect of FAM83H-AS1 knockdown in MDA-MB-468 cells [cellseq]

Project description:To investigate the role of lncRNA FAM83H-AS1 in breast cancer, we used shRNA to silence FAM83H-AS1 in MDA-MB-468 cells and performed RNA-seq analysis.

2026-02-01 | GSE289922 | GEO

FAM83H-AS1 is a non-coding oncogenic driver and therapeutic target of lung adenocarcinoma

Project description:Our study suggested that FAM83H-AS1 was a potential oncogenic driver due to chromosome 8q24 amplification in lung adenocarcinoma. To investigate the molecular mechanism of FAM83H-AS1, we performed high-thoughput RNA sequencing (RNA-Seq) assays after the silence of FAM83H-AS1 in A549 cell lines.

2020-10-20 | GSE159559 | GEO

Breast cancer cell MCF7+CYP1B1-AS1 LC-MS/MS

Project description:Long non-coding Rnas (lncRNAs) can act as oncogenes or tumor suppressors to regulate cancer development. We found that CYP1B1-AS1 was down-regulated in breast cancer tissues and correlated with the prognosis of patients. Lentiviral vectors were used to overexpress CYP1B1-AS1 in MCF7 cells, and the target proteins bound to CYP1B1-AS1 were detected by pulldown assay and mass spectrometry. The function of CYP1B1-AS1 is unknown. Our study revealed the molecular mechanism of CYP1B1-AS1 inhibiting breast cancer proliferation in breast cancer, and provided a new strategy for the treatment of breast cancer targeting lncRNA.

2023-10-24 | PXD037317 | Pride

Effect of FAM83H-AS1 knockdown in MDA-MB-468 cells [cellseq]

Project description:Effect of FAM83H-AS1 knockdown in MDA-MB-468 cells [cellseq]

| PRJNA1225303 | ENA

Proteomic analysis of Fam83h deficient and wild type ileum

Project description:We generated Fam83h-deficient mice (Fam83hem2(IMPC)Ccpcz, Fam83h-/-) and mice lacking a part of N-terminal CK1-binding domain (Fam83h∆87/∆87). Co-IP with anti-FAM83H antibody has confirmed the FAM83H–CK1 interaction in Fam83hwt/wt samples, which was absent in Fam83h-/- lysates. Additionally, samples from Fam83hΔ87/Δ87 mice were less likely to show FAM83H–CK1 interaction. Similarly, when CK1a antibody was used for pull downs, FAM83H–CK1 interaction was observed in Fam83hwt/wt lysates , but not in Fam83h-/- and Fam83hΔ87/Δ87 samples.

2025-09-08 | PXD064193 | Pride

FAM83H-AS1 is a non-coding oncogenic driver and therapeutic target of lung adenocarcinoma

Project description:FAM83H-AS1 is a non-coding oncogenic driver and therapeutic target of lung adenocarcinoma

| PRJNA669700 | ENA

RNA-sequencing reveals signaling pathway associated with cell adhesion in Fam83h-mutated cells

Project description:Truncation mutations in family with sequence similarity, member H (FAM83H) gene cause autosomal dominant hypocalcified amelogenesis imperfecta (ADHCAI). The aim of this study was to explore the effects of truncated FAM83H on enamel development. High throughput RNA-sequencing was used to detect the dysregulated signaling pathways in Fam83h-mutated LS8 cells. According to mRNA-sequencing, pathway related to cell adhesion was the most notably clustered in Fam83h-mutated cells. Immunofluorescence analysis further revealed decreased protein expression of desmoglein 3, a component of desmosomes, in Fam83h-mutated cells.

2024-01-28 | GSE195645 | GEO

MCF7 cells with LIFR knockdown

Project description:MCF7 cells were infected with lentiviral particles containing LIFR-targeted shRNAs then chemically selected to create a stable pooled population of shLIFR MCF7 cells. The goal of the study was to determine the downstream targets of LIFR in human MCF7 breast cancer cells.

2024-05-03 | GSE174592 | GEO

A long noncoding RNA landscape in breast cancer reveals a potential role for lncRNA AC009283.1 in proliferation and apoptosis in HER2-enriched molecular subtype

Project description:We silenced lncRNA AC009283.1 using shRNAs in cell line SKBR3, carried a ~75% silencing compared to thenegative control (NC). We evaluated the role of lncRNA AC009283.1 on oncogenic phenotypes in the HER2-enriched SKBR3 breast cancer cell line model. The knockdown of lncRNA AC009283.1 was achieved with ~75% of silencing efficiency. A complete transcriptomic analysis after silencing of lncRNA AC009283.1 revealed an impact on the global expression.

2020-08-12 | GSE134254 | 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