Ontology highlight
ABSTRACT:
PROVIDER: PRJNA256080 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression profiling in response to radiation treatment in human breast cancer
| PRJNA274283 | ENA
Project description:Gene expression profiling in response to radiation treatment in breast cancer [cell lines]
| PRJNA256082 | ENA
Project description:Gene expression profiling in response to radiation treatment in breast cancer [patient samples]
| PRJNA256081 | ENA
Project description:Breast tumors are characterized into different subtypes based on their surface marker expression, which affects their prognosis and treatment. For example, triple negative breast cancer cells (ER-/PR-/Her2-) show reduced susceptibility towards radiotherapy and chemotherapeutic agents. Poly (ADP-ribose) polymerase (PARP) inhibitors have shown promising results in clinical trials, both as single agents and in combination with other chemotherapeutics, in several subtypes of breast cancer patients. PARP1 is involved in DNA repair, apoptosis, and transcriptional regulation and an understanding of the effects of PARP inhibitors, specifically on metabolism, is currently lacking. Here, we have used NMR-based metabolomics to probe the cell line-specific effects of PARP inhibitor and radiation on metabolism in three distinct breast cancer cell lines. Our data reveal several cell line independent metabolic changes upon PARP inhibition, including an increase in taurine. Pathway enrichment and topology analysis identified that nitrogen metabolism, glycine, serine and threonine metabolism, aminoacyl-tRNA biosynthesis and taurine and hypotaurine metabolism were enriched after PARP inhibition in the three breast cancer cell lines. We observed that the majority of metabolic changes due to radiation as well as PARP inhibition were cell line dependent, highlighting the need to understand how these treatments affect cancer cell response via changes in metabolism. Finally, we observed that both PARP inhibition and radiation induced a similar metabolic response in the HCC1937 (BRCA mutant cell line), but not in MCF-7 and MDAMB231 cells, suggesting that radiation and PARP inhibition share similar interactions with metabolic pathways in BRCA mutant cells. Our study emphasizes the importance of differences in metabolic responses to cancer treatments in different subtypes of cancers.
2016-11-07 | MTBLS337 | MetaboLights
Project description:Gene expression response to high radiation treatment in MCF7 breast cancer cell line
| PRJNA268840 | ENA
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.
2015-10-31 | E-GEOD-59732 | biostudies-arrayexpress
Project description:Treatment of tumors with ionizing radiation for cancer therapy induces biological responses that include changes in cell cycle, activation of DNA repair mechanisms, and induction of apoptosis or senescence programs. What is not known is whether ionizing radiation induces an epigenetic DNA methylation response or whether epigenetic changes occur in genes in pathways classically associated with the radiation response. We exposed breast cancer cells to 0, 2, or 6 Gy and determined global DNA methylation at 1, 2, 4, 8, 24, 48, and 72 hours post-irradiation. We found that radiation treatment resulted in a DNA methylation response and that cell cycle, DNA repair, and apoptosis pathways were enriched in genes are were differentially-methylated. DNA methylation profiling of ionizing radiation treated cells using the Infinium HumanMethylation450 BeadChip.
2013-07-01 | E-GEOD-45958 | biostudies-arrayexpress
Project description:This study provides insights into the efficacy of beta-blockers as breast cancer therapeutics.Cell line models of basal-type and estrogen receptor-positive breast cancer were profiled for basal levels of adrenoceptor gene/protein expression, and ADRβ2-mediated cell behaviour including migration, invasion, adhesion, and proliferation in response to adrenoceptor agonist/antagonist treatment. Protein profiling and histology identified response biomarkers and drug targets. Protein profiling revealed the upregulation of the pro-metastatic gene LYPD3 in norepinephrine treated MDA MB 468 cells. Histology confirmed selective LYPD3 expression in clinical primary and metastatic breast tumours. These findings demonstrate that basal-type cancer models show a more aggressive ADRβ2-activated phenotype in the resting and stimulated state, which is attenuated by ADRβ2 inhibition, and explain some of the previous studies that have cast doubt on the value of beta-blocker therapy in breast cancer. These findings suggest that propranolol should be clinically evaluated in patients with basal-type tumours expressing high levels of ADRβ2 and LYPD3.
2020-05-26 | PXD009488 | Pride
Project description:Growing interest in the cellular origins of different breast cancer subtypes has prompted investigations into the subpopulations of the normal breast epithelia and their differentiation hierarchy. Several groups have demonstrated a likely luminal-progenitor cell origin for basal-like breast cancer. However, the molecular and cellular mechanisms underlying why one breast cell type might be more susceptible to transformation are yet to be elucidated. To observe the molecular differences in the different cell subpopulation response to ionizing radiation (IR), we performed gene expression profiling of MUC1+-sorted and CD10+-sorted primary human mammary epithelial cell cultures. Transcriptional response was measured at 2 and 24 hr after treatment with 2 and 5 Gy IR using Illumina HumanHT-12 v4 Expression Beadchips. The complete sample cohort included time-point matched untreated (0 Gy) controls in a total of 5 individual patients. Our analyses indicated several cell-type specific differences in response to IR. RNA was extracted from MUC1+-sorted and CD10+-sorted primary human mammary epithelial cell cultures at 2 and 24 hr after treatment with 0, 2, and 5 Gy ionizing radiation (12 samples per patient), in a total of 5 individual patients.
2016-02-07 | E-GEOD-67595 | biostudies-arrayexpress
Project description:We used charcoal-stripped serum on AR+ breast cancer cell lines to study the gene expression changes in the presence of androgens and/or radiation treatment in breast cancer.
2023-04-13 | GSE222992 | GEO