Proteomics

Dataset Information

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Multi-omics data integration reveals correlated regulatory features of triple negative breast cancer


ABSTRACT: Triple negative breast cancer is an aggressive type of breast cancer with very little treatment options. TNBC is very heterogeneous with large alterations in the genomic, transcriptomic, and proteomic landscapes leading to various subtypes with differing responses to therapeutic treatments. We applied a multi-omics data integration method to evaluate the correlation of important regulatory features in TNBC BRCA1 wild-type MDA-MB-231 and TNBC BRCA1 5382insC mutated HCC1937 cells compared with normal epithelial breast MCF10A cells. The data includes DNA methylation, RNAseq, protein, phosphoproteomics, and histone post-translational modification. Data integration methods identified regulatory features from each omics method had greater than 80% positive correlation within each TNBC subtype. Key regulatory features at each omics level were identified distinguishing the three cell lines and were involved in important cancer related pathways such as TGFbeta signaling, PI3K/AKT/mTOR, and Wnt/beta-catenin signaling.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Stephanie Byrum  

LAB HEAD: Stephanie D Byrum

PROVIDER: PXD025238 | Pride | 2021-06-24

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
Byrd_100719_PHOS_TMT1_SF01.raw Raw
Byrd_100719_PHOS_TMT1_SF02.raw Raw
Byrd_100719_PHOS_TMT1_SF03.raw Raw
Byrd_100719_PHOS_TMT1_SF04.raw Raw
Byrd_100719_PHOS_TMT1_SF05.raw Raw
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Publications


Triple negative breast cancer (TNBC) is an aggressive type of breast cancer with very little treatment options. TNBC is very heterogeneous with large alterations in the genomic, transcriptomic, and proteomic landscapes leading to various subtypes with differing responses to therapeutic treatments. We applied a multi-omics data integration method to evaluate the correlation of important regulatory features in TNBC BRCA1 wild-type MDA-MB-231 and TNBC BRCA1 5382insC mutated HCC1937 cells compared w  ...[more]

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