Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mechanistic Targets of Diallyl Trisulfide (DATS) in Human Breast Cancer Cells Identified by RNA-seq Analysis

ABSTRACT: We report differential gene expression changes by DATS in breast cancer cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE173616 | GEO | 2021/04/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Cancer-Selective Mechanistic Targets of Diallyl Trisulfide (DATS) in Human Breast Cancer Cells Identified by RNA-seq Analysis

Project description:We report differentially expressed genes by DATS exposure in MCF-10A human epithelial cell line and SK-BR-3 human breast cancer cell line

2022-04-20 | GSE200872 | GEO

Mechanistic Targets of Diallyl Trisulfide in Human Breast Cancer Cells Identified by RNA-seq Analysis.

Project description:Diallyl trisulfide (DATS), a metabolic by-product of processed garlic, is highly effective in inhibiting growth of human breast cancer cells in vitro and in vivo, but the underlying mechanisms are still not fully understood. In this study, we performed RNA-seq analyses using luminal-type (MCF-7) and basal-like (MDA-MB-231) human breast cancer cells to identify mechanistic targets of DATS. The Reactome Pathway Analysis revealed upregulation of genes associated with SLIT/ROBO tumor suppressor signaling following DATS treatment in both MCF-7 and MDA-MB-231 cells. However, the expression of SLIT2 and ROBO1 proteins or their downstream target C-X-C motif chemokine receptor 4 was not affected by DATS treatment in both cell lines. The Reactome as well as the Gene Ontology Pathways Analyses of the RNA-seq data from DATS-treated cells indicated downregulation of genes associated with G2/M phase cell cycle arrest in comparison with vehicle-treated control cells. Consistent with the RNA-seq data, DATS treatment caused a significant increase in the fraction of the G2/M population in both cell lines when compared to corresponding control cells. In addition, Ser10 phosphorylation of histone H3, a mitotic marker, was also increased significantly following DATS treatment in MCF-7 and MDA-MB-231 cells. These results indicate that while SLIT/ROBO signaling is not affected by DATS treatment, cell cycle arrest likely contributes to the antitumor effect of this phytochemical.

| S-EPMC8249207 | biostudies-literature

Novel cancer-selective and disease subtype-independent mechanistic targets of withaferin A in human breast cancer cells

Project description:We report differential gene expression changes by withaferin A in breast cancer cells versus a normal mammary epithelial cell line.

2020-09-17 | GSE158085 | GEO

Mechanistic Targets of Diallyl Trisulfide (DATS) in Human Breast Cancer Cells Identified by RNA-seq Analysis

Project description:Mechanistic Targets of Diallyl Trisulfide (DATS) in Human Breast Cancer Cells Identified by RNA-seq Analysis

| PRJNA726289 | ENA

Cancer-Selective Mechanistic Targets of Diallyl Trisulfide (DATS) in Human Breast Cancer Cells Identified by RNA-seq Analysis

Project description:Cancer-Selective Mechanistic Targets of Diallyl Trisulfide (DATS) in Human Breast Cancer Cells Identified by RNA-seq Analysis

| PRJNA827109 | ENA

Next Generation Sequencing of TGS24-treated human breast cancer cell line

Project description:We report the differential gene expression of TGS24-treated breast cancer cells

2022-03-06 | GSE168403 | GEO

Novel mechanistic targets of forkhead box Q1 transcription factor in human breast cancer cells.

Project description:The transcription factor forkhead box Q1 (FoxQ1) is overexpressed in different solid tumors including breast cancer, but the mechanism underlying its oncogenic function is still not fully understood. In this study, we compared RNA-seq data from FoxQ1 overexpressing SUM159 cells with that of empty vector-transfected control cells to identify novel mechanistic targets of this transcription factor. Analysis of The Cancer Genome Atlas (TCGA) data set revealed significantly higher expression of FoxQ1 in black breast cancer patients compared with white women with this disease. In contrast, expression of FoxQ1 was comparable in ductal and lobular carcinomas in the breast cancer TCGA data set. Complementing our published findings in basal-like subtype, immunohistochemistry revealed upregulation of FoxQ1 protein in luminal-type human breast cancer tissue microarrays when compared with normal mammary tissues. Many previously reported transcriptional targets of FoxQ1 (eg, E-cadherin, N-cadherin, fibronectin 1, etc) were verified from the RNA-seq analysis. FoxQ1 overexpression resulted in the downregulation of genes associated with cell cycle checkpoints, M phase, and cellular response to stress/external stimuli as evidenced from the Reactome pathway analysis. Consequently, FoxQ1 overexpression resulted in mitotic arrest in basal-like SUM159 and human mammary epithelial cell line, but not in luminal-type MCF-7 cells. Finally, we show for the first time that FoxQ1 is a direct transcriptional regulator of interleukin (IL)-1α, IL-8, and vascular endothelial growth factor in breast cancer cells as evidenced by chromatin immunoprecipitation assay. In conclusion, the present study reports novel mechanistic targets of FoxQ1 in human breast cancer cells.

| S-EPMC7484420 | biostudies-literature

Identifying novel anti-angiogenic targets in human breast cancer

Project description:We analysed gene expression in normal breast blood vessels and breast invasive ductal carinoma blood vessels.

2012-08-03 | GSE31138 | GEO

Identifying novel anti-angiogenic targets in human breast cancer

Project description:We analysed gene expression in normal breast blood vessels and breast invasive ductal carinoma blood vessels. Normal breast sections and IDC breast sections were immunostained for endothelial-specific CD31. Vessels were dissected and captured with laser capture microscopy, and RNA was extracted and analysed on an Affymetrx array chip. In total, gene expression in blood vessels from 3 normal breast and 3 IDC breast was analysed.

2012-08-02 | E-GEOD-31138 | biostudies-arrayexpress

RNA-seq reveals novel cancer-selective and disease subtype-independent mechanistic targets of withaferin A in human breast cancer cells.

Project description:Withaferin A (WA) exhibits cancer chemopreventive efficacy in preclinical models representative of two different subtypes of breast cancer. However, the mechanism(s) underlying breast cancer chemoprevention by WA is not fully elucidated. We performed RNA-seq analyses using a non-tumorigenic mammary epithelial cell line (MCF-10A) and human breast cancer cells (BCC) belonging to the luminal-type (MCF-7), HER2-enriched (SK-BR-3), and basal-like subtype (MDA-MB-231) to identify novel cancer-selective mechanistic targets of WA. The WA-regulated transcriptome was strikingly different between MCF-10A versus BCC. The Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed downregulation of genes associated with cellular senescence in WA-treated BCC. Consequently, the number of senescence-associated β-galactosidase positive cells was decreased significantly in WA-treated BCC but not in the MCF-10A cells. WA treatment caused upregulation of senescence marker p21 more robustly in BCC than in MCF-10A. Breast cancer prevention by WA in rats was also associated with upregulation of p21 protein expression. The Reactome pathway analyses indicated upregulation of genes associated with cellular response to stress/external stimuli in WA-treated BCC but not in MCF-10A. Two proteins represented in these pathways (HSPA6 and NRF2) were further investigated. While HSPA6 was dispensable for WA-mediated apoptosis and autophagy or inhibition of cell migration, the NRF2 knockout cells were more resistant to apoptosis resulting from WA treatment than control cells. Finally, expression of some glycolysis-related proteins was decreased by WA treatment both in vitro and in vivo. In summary, this study provides novel insights into cancer-selective pathways affected by WA that may contribute to its chemopreventive efficacy in breast cancer.

| S-EPMC7736309 | biostudies-literature

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