Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of WFDC21P knockdown in BT549 cells.

ABSTRACT: We identify a long noncoding RNA, WFDC21P (lnc-DC), which corelates to anti-tumor immunity in triple negative breast cancer (TNBC). To investigate the pathway that mediates the role of WFDC21P in TNBC, we knock down WFDC21P in BT549 cells with two siRNAs and perform RNA-seq analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE303355 | GEO | 2026/03/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression data from BT549 attached/suspended cells

Project description:Cells grown in forced suspension culture mimic the early steps of metastasis. In order to determine what might be driving the ability of TNBC cells to survive in suspension, a global gene expression profiling experiment was performed. Human triple negative breast cancer (TNBC) cell line BT549 was grown in attached or forced suspension conditions for 24 hours, then RNA was harvested to look for changes in global gene expression.

2017-03-01 | GSE95472 | GEO

miR-200c induction in BT549 TNBC cells

Project description:miR-200c induction in BT549 TNBC cells

| PRJNA423021 | ENA

Genome wide SOX4 specific binding sites in BT549 human TNBC cells

Project description:We identified the SOX4 transcription factor and integrin alpha V encoded by the ITGAV gene as important resistance mechanisms to T cell-mediated cytotoxicity of TNBC cells. Here, we performed RNA seq. analysis of SOX4 and ITGAV deficient (CRISPR knockout) BT549 human and 4T1 murine TNBC cells as compared to control edited counterparts. Additionally, we performed SOX4 specific ChIP-seq studies in BT549 human TNBC cells. The objective of the study was to identify the molecular regulators and signaling pathways that mediate resistance to T cell mediated immunity. GSEA analysis of RNA-seq data showed that the 'interferon response' represented one of the top pathways for genes upregulated in SOX4 or ITGAV edited compared to control TNBC cells. In contrast, gene sets associated with TGF beta and TNF alpha/NF kappa b were negatively enriched in both Sox4 and Itgav edited TNBC cells. Further analysis of RNA-seq data showed that SOX4 or ITGAV edited TNBC cells contained higher mRNA levels of many interferon-stimulated genes (ISGs), including genes associated with important innate immune pathways such as RIG-I/MDA-5, cGAS - STING and the AIM2 inflammasome

2021-01-01 | GSE144012 | GEO

Insights into the invasiveness of triple negative breast cancer from genome-wide profiling of transcription factor AP-1 (expression)

Project description:Triple negative breast cancer (TNBC) is an aggressive clinical phenotype, and accounts for 15% to 20% of all breast cancers. The molecular determinants of malignant cell behaviors in TNBC remain largely unknown. We find that the AP-1 transcription factor component, Fra-1, is overexpressed in basal-like breast tumors, and its expression level has high prognostic significance. Depletion of Fra-1 or its heterodimeric partner c-Jun inhibits the proliferative and invasive phenotypes in TNBC cells. To gain insights into the transcriptional regulatory networks of AP-1 in TNBC cells, we combine genome-wide ChIP-seq with loss-of-function transcriptome analyses. We observe dysregulation of direct targets of the Fra-1/c-Jun heterodimer involved in cell proliferation, cell adhesion, and cell-cell contact. Intriguingly, we find that AP-1 mediates downregulation of E-cadherin through direct transcriptional induction of ZEB2. This work sheds light on the mechanisms and pathways by which TNBC acquires invasiveness and proliferative propensity. BT549 cells grown in complete medium were transfected with a control siRNA, siRNA targeting Fra-1 or siRNA targeting c-Jun for 72 h, and then global gene expression profiles were assessed. Three or four biological replicates were used for each group.

2014-06-30 | E-GEOD-46440 | biostudies-arrayexpress

Transcriptome analysis of BT549 cells overexpressing SNHG15

Project description:LncRNA SNHG15 is an oncogenic lncRNA in a variety of cancers including breast cancer, lung cancer, and hepatocellular carcinoma. To screen genes regulated by SNHG15, we performed RNA-seq with stable SNHG15-overexpression BT549 cells, using BT549-pcIP2 as control.

2023-06-08 | GSE220492 | GEO

Screening lncRNAs that binding with catenin.

Project description:Because of its insensitivity to existing radiotherapy, namely chemotherapy and targeted treatments, triple-negative breast cancer (TNBC) remains a great challenge to overcome. Increasing evidence has indicated abnormal Wnt/β-catenin pathway activation in TNBC but not luminal or HER2+ breast cancer, and lncRNAs play a key role in a variety of cancers. Through lncRNA microarray profiling between activated and inactivated wnt/β-catenin pathway of TNBC tissues, lnc-WAL (wnt/β-catenin associated lncRNA; WAL) was selected as the top upregulated lncRNA in wnt/β-catenin pathway activation compared with the inactivation group. RIP-seq was used to compare the β-catenin and IgG groups, where lnc-WAL could interact with β-catenin. Clinically, increased lnc-WAL in TNBC tumor tissue was associated with shorter survival. lnc-WAL promoted EMT, the proliferation, migration and invasion of breast cancer stem cells (BCSCs), and TNBC cells. Mechanistically, lnc-WAL inhibited β-catenin protein degradation via Axin-mediated phosphorylation at serine 45. Subsequently, β-catenin accumulated in the nucleus and activated the target genes. Importantly, wnt/β-catenin pathway activation stimulated the transcription of lnc-WAL. These results pointed to a master regulatory role of lnc-WAL/Axin/β-catenin in the malignant progression of TNBC. Our findings provide important clinical translational evidence that lnc-WAL may be a potential therapeutic target against TNBC.

2025-05-24 | GSE268287 | GEO

Genome wide SOX4 specific binding sites in BT549 human TNBC cells

Project description:Genome wide SOX4 specific binding sites in BT549 human TNBC cells

| PRJNA602503 | ENA

Transcript sequencing data in BT549 cell line.

Project description:To explore the DEGs in BT549 cell line treated with ENL.

2024-12-23 | GSE272946 | GEO

BT549 cells with control or NFIL3 shRNA treatment

Project description:Transcriptional profiling with samples from BT549 cells that were infected with control or NFIL3 shRNA

2012-09-02 | GSE31425 | GEO

miR-200c induction in BT549 TNBC cells

Project description:We performed microarray analysis on BT549 cells that express miR-200c in a doxycycline (dox)-inducible manner from the miR-200c-TripZ system.

2017-12-20 | GSE108271 | 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