Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Study of gene targets regulated by oncogenic PIK3CA and/or Her2

ABSTRACT: Mutant PIK3CA and Her2 genes are oncogenic and their co-existence in breast cancer has been well identified. However, the gene targets and cell signalling pathway regulated by mutant PIK3CA, Her2 and both of PIK3CA and Her2 have not been well studied. We established stable cell models through transfecting mutant PIK3CA, Her2 and both mutant PIK3CA and Her2 into MCF10A cells and performed Affymetrix microarray to identify downstream target genes controlled by either mutant PIK3CA, Her2 or both PIK3CA and Her2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE99512 | GEO | 2017/06/01

SECONDARY ACCESSION(S): PRJNA388678

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Development of gene expression signatures for MCF10A cell lines carrying HER2 and WT or H1047R PIK3CA oncogenes.

Project description:We wanted to know how introduction of H1047R oncogenic mutation of PIK3CA (p110a subunit of PI3K) in HER2-overexpressing MCF10A human non-transformed mammary epitheial cell lines introduces change in gene expression levels. Our control was HER2-overexpressing MCF10A cell line with wild-type (WT) PIK3CA. Mutated oncogene-induced gene expression signature was measured and compared with that induced by the WT oncogene from cell lines harvested at 70-80% confluency.

2021-03-16 | GSE117389 | GEO

Expression data from HER2 L755S, PIK3CA E545K, and co-cultured cells in the MCF-10A background

Project description:When co-cultured, HER2 L755S mutant cells are induced to proliferate when coming into close contact with PIK3CA E545K mutant cells We used a microarray to compare transciptome-wide expression levels between HER2 L755S cells, PIK3CA E545K cells, and co-cultures containing both cell types.

2021-03-18 | GSE165065 | GEO

Global proteomic alterations in extracellular vesicles induced by oncogenic PIK3CA mutations

Project description:MCF10A cells, and two isogenic mutant cell lines with known mutations in PIK3CA (E545 K and H1047R) were cultured in triplicate using culture medium depleted of extracellular vesicles. Cell culture supernatants were collected to study the extracellular vesicles (EVs) released by these cells. EVs were isolated from the samples by ultracentrifugation and their proteins digested. The resulting peptides were labeled with TMT and analyzed by mass spectrometry to identify differentially expressed proteins.

2023-10-22 | PXD031718 | Pride

Mutant PI3K cooperates with HER2 to promote mammary tumor formation and induces trastuzumab resistance in vivo

Project description:HER2 (ERBB2) gene amplification and PIK3CA mutations often co-occur in breast cancer, and aberrant activation of the PI3K pathway has been implicated in resistance to HER2-directed therapies. We have created a mouse model of HER2-overexpressing (HER2+), PIK3CAH1047R-mutant breast cancer. Mice expressing both human HER2 and mutant PIK3CA in their mammary glands developed tumors with a significantly shorter latency compared to mice expressing either oncogene alone. By microarray analysis, HER2-driven tumors clustered with the luminal subtype, whereas HER2+PIK3CA and PIK3CA-driven tumors were associated with the claudin-low breast cancer subtype. In accordance, PIK3CA and HER2+PIK3CA tumors expressed elevated levels of EMT and stem cell markers, and cells from HER2+PIK3CA tumors more efficiently formed mammospheres, providing further evidence that activated PIK3CA may enrich for cancer stem cells. Finally, HER2+PIK3CA tumors are resistant to the HER2 antibody trastuzumab; resistance is partially reversed by the addition of a PI3K inhibitor. Taken together, these studies suggest that the co-expression of HER2 and PI3KH1047R in the mouse mammary gland accelerates the formation of aggressive, trastuzumab-resistant tumors. referenceXsample

2013-09-03 | E-GEOD-41118 | biostudies-arrayexpress

Mutant PI3K cooperates with HER2 to promote mammary tumor formation and induces trastuzumab resistance in vivo

2013-09-03 | GSE41118 | GEO

Phosphoproteomic analysis of breast epithelial cells with isogenic knockin of PIK3CA mutations

Project description:The PIK3CA gene is frequently mutated in human cancers. To study the signaling mechanisms responsible for cell growth and invasion phenotypes induced by mutant PIK3CA molecules, we carried out a SILAC-based quantitative phosphoproteomic analysis of MCF10A, a spontaneously immortalized normal mammary epithelial cell line, and two MCF10A knockin cell lines containing different activating mutations of the PIK3CA gene. MCF10A and PIK3CA mutation knock in cells were propagated in DMEM/F12 SILAC media deficient in both L-lysine and L-arginine and supplemented with light lysine (K) and arginine (R) for light, 2H4-K and 13C6-R for medium state and 13C615N2-K and 13C615N4-R for heavy state labeling. Cell lysates were prepared in urea lysis buffer containing 20 mM HEPES pH 8.0, 9 M urea, 1 mM sodium orthovanadate, 2.5 mM sodium pyrophosphate, 1 mM ß-glycerophosphate and 5mM sodium fluoride. The lysates were reduced, alkylated and digested by trypsin. Tryptic peptides were desalted by C18 reverse phase column and followed by strong cation exchange (SCX) fractionation. Fractionated peptides were subjected to TiO2-based phosphopeptide enrichment. LC-MS/MS analysis of enriched phosphopeptides was carried out using a reverse-phase liquid chromatography system interfaced with an LTQ-Orbitrap Velos mass spectrometer. Proteome Discoverer (v 1.3) suite was used for quantitation and database searches. The tandem mass spectrometry data were searched using Mascot (2.2.0) and SEQUEST search algorithms against a Human RefSeq database supplemented with frequently observed contaminants.

2015-07-28 | PXD000599 | Pride

Proteomic Analysis of wild-type and PIK3CA mutant cell lines

Project description:Wild-type and PIK3CA mutant MCF10A cell lines were analyzed using shotgun proteomics to identify proteins that were altered by either 545K or H1047R PIK3CA mutations. Cell lines were digested and fractionated using isoelectric focusing and peptides were analyzed using LC-MS/MS analysis.

2015-03-05 | MSV000079060 | MassIVE

Transcriptional landscape of oncogenic PI3K

Project description:RNA-seq performed in triplicates in MCF10A and MEF cells. Wildtype/parental vs PIK3CA H1047R mutant. MEFs were treated with DMSO or GDC0032 (500nM) PI3Ka inhibitor treatment while MCF10A cells were treated with DMSO or alpelisib (BYL719) at 1uM.

2022-04-25 | GSE157858 | GEO

Characterising early phosphorylation events upon HER2 protein overexpression

Project description:HER2 transduced cells which we will refer to as HER2-DOX –. These cells are 99% GFP positive (i.e., 99% cells have HER2 transduced, un-induced). As a control, we had GFP empty vector transduced MCF10A cells (95% have GFP transduced). Both cell types in triplicates. We had 4 time-points 0h, 30 mins, 4hours, and 7 hours (time duration for which HER2 will be induced). DOX was added to the GFP-MCF10A cells as a control. Only 1ug/ml of DOX was be used.

2023-01-23 | PXD034105 | Pride

Pentraxin-3 is a PI 3-Kinase Effector that Regulates Stem-Cell-Like Traits in Basal-Like Breast Cancer

Project description:MCF10A cells: control vs. PIK3CA mutant (H1047R) Transcriptional profiling of MCF10A comparing control (expressing JP1520-PIK3CA-WT; Addgen plasmid #14570) and PIK3CA mutant (JP1520-PIK3CA-H1047R; Addgene plasmic#14572). Goal was to determine the effects of the PIK3CA H1047R mutation in the on global gene expression in MCF10A cells.

2017-02-28 | GSE93422 | 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