Expression data from Breast cancer subtypes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Fatima Mechta-Grigoriou
PROVIDER: E-GEOD-45827 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Introduction: Breast radiotherapy is currently â??one size fits allâ?? regardless of breast cancer subtype (eg. luminal, basal). However, recent clinical data suggests that radiation response may vary significantly among subtypes. Therefore, current practice leads to over- or under-treatment of women whose tumors are more or less radiation responsive. We hypothesized that this clinical variability may be due, in part, to differences in cellular radiation response. Methods: We exposed 16 biologically-diverse breast tumor cell lines to 0 or 5GY radiation. Microarray analysis was performed on RNA harvested from those cell lines. Samples were run in triplicate. Following quality assessment, differential gene expression analysis was performed using a two-way multiplicative linear mixed-effects model. A candidate radiation response biomarkers with biologically plausible role in radiation response, were identified and confirmed at the RNA and protein level with qPCR and Western blotting assays. Induction in human breast tumors was confirmed in 32 patients with paired pre- and post-radiation tumor samples using IHC and microarray analysis. Quantification of protein was performed in a blinded manner and included positive and negative controls. The objective of our study was to identify genomic determinants of radiation sensitivity using clinical samples as well as breast tumor cell lines. In order to identify differences in the radiation response gene expression profiles of specific breast cancer subtypes, we exposed 16 biologically-diverse breast tumor cell lines to 0 or 5GY radiation. Microarray analysis was performed on RNA harvested from those cell lines. Samples were run in triplicate. Following quality assessment, differential gene expression analysis was performed using a two-way multiplicative linear mixed-effects model. Candidate radiation response biomarker with a biologically plausible role in radiation response, were identified and confirmed at the RNA and protein level with qPCR and Western blotting assays. Induction of the genes of interest were further evaluated and confirmed in human breast tumors in 32 breast cancer patients with paired pre- and post-radiation tumor samples using IHC and microarray analysis assays.
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Project description:Emerging evidences indicate a new role of TFPI in cancer biology. We recently reported that both isoforms of TFPI induced apoptosis and inhibited proliferation of cancer cells. The signaling pathway(s) mediating the effects of TFPI is, however, presently still unclear. Our goal was to further investigate the cellular processes affected by TFPI and to get insight into the molecular mechanisms involved in the effects of TFPI, using a global gene expression study approach. TFPIa or TFPIb cDNA were transfected into SK-BR-3 breast cancer cells for stable overexpression. Global mRNA and microRNA (miRNA) expressions were measured and functional annotation of the differentially expressed genes and miRNAs according to gene ontology terms was conducted. Selected results were validated using qRT-PCR and Western blot. Overexpression of TFPIa or TFPIb resulted in a 6.4- and 17-fold increase in TFPI protein levels, respectively. A total of 242 and 801 mRNA transcripts and 120 and 46 miRNAs were differentially expressed in cells overexpressing TFPIa or TFPIb, respectively. Overexpression of either isoform significantly affected the expression of genes involved in cell development (apoptosis, cell movement, migration, invasion, colony formation, growth, and adhesion) and immune response. Network analyses revealed biological interactions between these genes and implied that several of the genes may be involved in both processes. Functional cluster analyses indicated altered activity of the epidermal growth factor receptor (EGFR), small GTPases, and the NFkB and JAK/STAT cascades. Integrated mRNA-miRNA analyses showed that up to 46 and 252 genes differentially expressed in cells overexpressing TFPIa or TFPIb, respectively, may have been regulated by miRNAs. Overexpression of TFPI in breast cancer cells affected the expression of mRNAs and miRNAs involved in processes facilitating cancer cell growth and immunologic response, probably by signal transduction involving the EGFR pathway. Total RNA was isolated from SK-BR-3 breast cancer cells stably transfected with TFPIalpha or TFPIbeta cDNA, or with an empty vector for control. RNA was obtained from three independent isolations, yielding three biological replicates of each of the three samples. Mean expression data from cells overexpressing TFPIalpha or TFPIbeta were compared to mean data from cells transfected with an empty vector.
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