Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HT-29 mouse xenograft mediated proteomic profiling of metabolic proteins as potential biomarkers of radioresponsiveness for colorectal cancer

ABSTRACT: Using a mouse model inoculated with human CRC cells (HT-29-Red-Fluc), we have shortlisted some specific metabolic proteins that are differentially expressed in tumours that responded well to radiation treatment.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Dr. Helen Ka Wai LAW

PROVIDER: MSV000089307 | MassIVE | Mon Apr 25 01:17:00 BST 2022

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of sodium butyrate on colorectal cancer cell line HT-29

Project description:Analysis of colorectal cancer (CRC) cell line HT-29 treated with Sodium Butyrate. Sodium Butyrate, a HDAC inhibitor present in gut, can differentiate the undifferentiated HT-29 to enterocytes by the induction of brush border enzyme alkaline phosphatase. Results provide the transcriptional profiling underlying the butyrate-induced differentiation of CRC.

2016-12-31 | GSE61429 | GEO

ZEB1-mediated Epithelial to Mesenchymal Transition in Colorectal cancer HT-29 cell line

Project description:We report the induction of epithelial-mesenchymal transition (EMT) in the epithelial colorectal cancer (CRC) cell line HT-29. ZEB1 expression is sufficient to induce the downregulation of epithelial markers such as E-cadherin, claudins, keratins and occludin, while upregulating the expression of several mesenchymal markers such as vimentin and fibronectin.

2025-12-01 | GSE276336 | GEO

LARGE2 mediates O-glycosylation in HT-29 colorectal cancer cells

Project description:The O-glycosyltransferase LARGE2 attaches a laminin-binding matriglycan structure on alpha-Dystroglycan (α-DG) to mediate the interaction of different cell types with their laminin-containing basement membrane. We used HT-29 CRC cells, characterized by low endogenous LARGE2 gene expression, to ectopically express LARGE2 and to drive O glycosylation of its protein substrates. Immunoblot analyses had revealed that the addition of matriglycan-structures on LARGE2 substrate proteins substantially increased their molecular weight (MW). In order to take into account this shift in MW of candidate proteins, glycoprotein-enriched fractions from HT-29 cells with or without ectopic LARGE2 expression were separated by gel electrophoresis and subsequently fractionated in 6 different molecular weight windows (kDa: 0-25, 25-55, 55-75, 75-110, 110-160, 160<). Subsequently, samples were prepared for quantitative mass spectrometry analysis (qLC-MS/MS) analysis according to standard procedures. qLC-MS-MS analysis identified α-DG–related peptides within higher MW protein fractions only when LARGE2 was overexpressed. HT-29 cell secreted Laminin-2 was exclusively detected together with these high MW forms of α-DG, which demonstrated the affinity of Laminin towards the LARGE2-synthesized matriglycan structure on α-DG. Additional candidate proteins identified in this study need further experimental confirmation. Overall, we show that size fractionation after gel electrophoresis followed by quantitative mass spectrometry, performed separately on different MW windows, represents an elegant approach to reveal potential substrates of the O-glycosyltransferase LARGE2.

2020-06-28 | PXD013800 | Pride

Expression data of colorectal cancer HT-29 cells

Project description:Colorectal cancer HT-29 cell line is a comonly-used human cancer cell line. We have used this cell line for examining the effect of various anticancer compounds on gene expression and we obtained gene expression data of untreated HT-29 cells as a control data for the analysis.

2017-06-14 | GSE99968 | GEO

HT-29 and SW620

Project description:HT-29 and SW620

| PRJNA1200001 | ENA

RNA-seq in HT-29 colorectal cancer cells after F. nucleatum treatment

Project description:To elucidate whether F. nucleatum plays a role in colorectal cancer tumorigenesis, RNA-seq analysis was performed to compare the gene expression profiles of F. nucleatum treated HT-29 cell line or not.

2017-07-28 | GSE90944 | GEO

Modulated electro-hyperthermia related mRNA expression profile development in HT-29 xenograft mouse model.

Project description:HT-29 human colorectal adenocarcinoma cells were xenografted into both femoral regions of 6 to 8-week old Balb/c (nu/nu) mice. After 18 days electromagnetic heat treatment was performed. We used microarray technology to identify the heat treatment releted gene expression alterations using human tumor xenograft mouse model.

2014-09-01 | GSE58750 | GEO

Expression data from human HT-29 immortalized colorectal adenocarcinoma cell line

Project description:Gene expression profiling for identification of genes regulated by DNA methylation Total RNA was extracted from HT-29 cell line was hybridized on Affymetrix HGU133 Plus 2.0 microarrays

2012-01-01 | E-GEOD-29060 | biostudies-arrayexpress

Proteomic and phosphoproteomic analyses for HT-29

Project description:Metastatic BRAFV600E colorectal cancer (CRC) confers poor prognosis and run into a bottleneck in the current treatment strategies. To identify regulatory pathways independent of the MAPK pathway in BRAFV600E CRC, we performed CRISPR-Cas9 screening, and and find targeting glutathione peroxidase 4 (GPX4) remarkably overcome BRAF inhibitor (BRAFi) ± epidermal growth factor receptor (EGFR) inhibitor (EGFRi) resistance in BRAFV600E CRC. Specifically, BRAFi ± EGFRi induced GPX4 upregulated expression and antagonized ferroptosis. Moreover, polo-like kinase 1 (PLK1) substrate activation promoted PLK1 translocation to the nucleus, activating chromobox protein homolog 8 (CBX8) phosphorylation at Ser265, which induce GPX4 expression. Targeting PLK1 promoted BRAFi ± EGFRi inhibition and triggered ferroptosis in vitro, vivo, organoid, and patient-derived xenograft model. Collectively, we demonstrate a novel PLK1–CBX8–GPX4 signaling axis relaying the ferroptosis mechanism of therapeutic resistance operated independent of MAPK signaling and suggest a clinically actionable strategy to overcome BRAFi ± EGFRi resistance in BRAFV600E CRC.

2025-02-28 | PXD058218 | Pride

RAMPAGE from HT-29 (ENCSR295GUQ)

Project description:The libraries contained in this experiment come from independent growths of cell line HT-29. They are stranded PE101 Illumina Hi-Seq RAMPAGE libraries from rRNA-depleted Total RNA > 200 nucleotides in size. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf

2016-11-08 | GSE88168 | 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