Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Knock-in of oncogenic KRAS mutations in MCF-10A

PROVIDER: PRJNA526932 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8725740_1.fastq.gz	Fastqsanger.gz
	SRR8725740_2.fastq.gz	Fastqsanger.gz
	SRR8725739_1.fastq.gz	Fastqsanger.gz
	SRR8725739_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

NFIB Is a Pioneer Factor for DNA Replication by Acting as a Genome Organizer [WGS]

Project description:Whole genome sequencing (WGS) of MCF-10A cells without or with NFIB overexpression cultured at 30 or 75 days and 5-fluoracil-resistant or oxaliplatin-resistant MCF-10A cells with NFIB overexpression cultured at 75 days to investigate whether the oncogenic potential of NFIB is linked to its function in replication initiation.

2023-08-22 | GSE201866 | GEO

Genome-wide analysis of gene expression by miR-204/211 in normal breast cell line MCF10A and breast cancer cell line MCF7

Project description:Genome-wide expression analysis of MCF-10A and MCF-7 where miR-204 and miR-211 are overexpressed. The characteristics of differentially expressed genes in both cell lines derives the cells toward being oncogenic.

2016-05-23 | GSE75292 | GEO

Homo sapiens

Project description:Knock-in of PIK3CA-H1047R into MCF-10A

| PRJNA267827 | ENA

Gene expression changes caused by KRAS in MCF-10A

Project description:Gene expression changes caused by KRAS in MCF-10A

| PRJNA527306 | ENA

Gene expression signatures associated with PI3Kα-induced senescence

Project description:To investigate the mechanisms of PI3Kα-induced senescence, we performed a gene expression microarray analysis with MCF-10A/H and parental MCF-10A cells.

2018-11-28 | GSE123014 | GEO

MicroRNA-7-5p mediates the anti-oncogenic effect of hepatocyte growth factor in the MCF-10A mammary epithelial cell

Project description:Genome wide expression profiling of breast normal cell line MCF-10A. The Illumina HumanHT-12 v4 Expression BeadChip was used to obtain expression profiles. This profiling indicates that MicroRNA-7 mediates the activity of HGF to suppress oncogenic proteins, which inhibits cancer progress.

2017-12-06 | GSE102758 | GEO

Knock-in of PIK3CA-H1047R into MCF-10A

Project description:We have compared the proteome, transcriptome and metabolome of two isogenic cell lines: MCF-10A, derived from human breast epithelium, and the mutant MCF-10A-H1047R. These cell lines differ by a single amino acid substitution (H1047R) caused by single nucleotide change in one allele of the PIK3CA gene which encodes the catalytic subunit p110α of phosphatidylinositol 3-kinase (PI3K). The H1047R mutation of PIK3CA is one of the most frequently encountered somatic cancer-specific mutations. In MCF-10A, this mutation induces an extensive cellular reorganization that far exceeds the known signaling activities of PI3K. The changes are highly diverse; with examples in structural protein levels, the DNA repair machinery and sterol synthesis. Gene set enrichment analysis reveals a highly significant concordance of the genes differentially expressed in MCF-10A-H1047R cells and the established protein and RNA signatures of basal breast cancer. No such concordance was found with the specific gene signatures of other histological types of breast cancer. Our data document the power of a single base mutation, inducing an extensive remodeling of the cell toward the phenotype of a specific cancer.

2015-01-19 | GSE63452 | GEO

Small RNAs subcellular distribution in breast cancer and normal cell lines

Project description:We detect the small RNAs subcellular distribution in breast cancer cell lines MCF-7 and MDA-MB-231, and normal cell line MCF-10A.

2009-06-16 | GSE15937 | GEO

Targeting cancer with small molecule pan-KRAS degraders

Project description:Despite the high prevalence of cancers driven by KRAS mutations, to date only the G12C mutation has been clinically proven to be druggable via covalent targeting of the mutated cysteine amino acid residue1. However, in many cancer indications other KRAS mutations, such as G12D and -V, are far more prevalent and small molecule concepts that can address a wider variety of oncogenic KRAS alleles are in high clinical demand2. Here we show that a single small molecule can be used to simultaneously and potently degrade 13 out of 17 of the most prevalent oncogenic KRAS alleles, including those not yet tractable by inhibitors. Compared with inhibition, degradation of oncogenic KRAS results in more profound and sustained pathway modulation across a broad range of KRAS mutant cell lines. As a result, KRAS degraders inhibit growth of the majority of cancer cell lines driven by KRAS mutations while sparing models without genetic KRAS aberrations. Finally, we demonstrate that pharmacological degradation of oncogenic KRAS leads to tumour regression in vivo. Together, these findings unveil a new path towards addressing KRAS driven cancers with small molecule degraders. This is the proteomics analysis of ACBI3 and compoun 8, its negative control.

2024-10-01 | PXD050650 | Pride

Targeting cancer with small molecule panKRAS degraders

Project description:Despite the high prevalence of cancers driven by KRAS mutations, to date only the G12C mutation has been clinically proven to be druggable via covalent targeting of the mutated cysteine amino acid residue. However, in many cancer indications other KRAS mutations, such as G12D and -V, are far more prevalent and small molecule concepts that can address a wider variety of oncogenic KRAS alleles are in high clinical demand. Here we show that a single small molecule degrader can be used to simultaneously and potently target multiple KRAS alleles, including those not yet tractable by inhibitors. Degradation of oncogenic KRAS results in profound and sustained pathway modulation across a broad range of KRAS mutant cell lines. As a result, KRAS degraders inhibit growth of the majority of cancer cell lines driven by KRAS mutations while sparing models without genetic KRAS aberrations. Finally, we demonstrate that pharmacological degradation of oncogenic KRAS leads to tumour regression in vivo. Together, these findings unveil a new path towards addressing KRAS driven cancers with small molecule degraders. This experiment corresponds to Figure 2g

2024-10-01 | PXD045460 | Pride

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