Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA187147 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome sequencing from MCF-7 breast cancer cell line
| PRJNA33237 | ENA
Project description:Identification of KDM3A regulated genes in the ER positive breast cancer cell line MCF-7
| PRJNA284106 | ENA
Project description:Previously, we have shown that HIST1H2ac is overexpressed in MCF-7 breast cancer cell line. It acts as a master regulator of estrogen receptor alpha-dependent gene expression in ER+ breast cancer cells. In the present study, we investigate the genome-wide protein DNA-binding events of HIST1H2ac protein in MCF-7 breast cancer cell line by over-expressing hemagglutinin (HA)-tagged HIST1H2ac and compared with MCF-7 cells over-expressing HA. The protein-bound DNA was recovered by immunoprecipitation using anti-HA antibody. The ChIP DNA and input DNA were sequenced with an Illumina HiSeq 2000 sequencer.
2016-05-19 | E-MTAB-3160 | biostudies-arrayexpress
Project description:Full-length transcripts of the MCF-7 breast cancer cell line
| PRJNA277461 | ENA
Project description:INPP4B over-expressed INPP4B MCF-7 luminal breast cancer cell line
2020-06-01 | MSV000085526 | MassIVE
Project description:ZNF703 overexpression and/or knockdown in the breast cancer cell line MCF-7
| PRJNA130809 | 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:Cancer genomes are characterized by accumulation of small-scale somatic mutations as well as large-scale chromosomal deletions, amplifications, and complex structural rearrangements. This characteristic is at least partially dependent on the ability of cancer cells to undergo recurrent chromosome breakage. In order to address to what extent chromosomal structural rearrangement breakpoints correlate with recurrent DNA double strand breaks (DSBs), we simultaneously mapped chromosome structural variation breakpoints by whole genome DNA-seq and spontaneous DSB formation by Break-seq in the breast cancer cell line MCF-7 and a non-cancer control cell line MCF-10A. We identified concurrent DSBs and structural variation breakpoints almost exclusively in the pericentromeric region of chromosome 16q in MCF-7 cells. We fine-tuned the identification of copy number variation breakpoints on 16q. In addition, we detected recurrent DSBs that occurred in both MCF-7 and MCF-10A. We propose a model for DSB-driven chromosome rearrangements that led to the translocation of 16q, likely with 10q, and the eventual 16q loss that does not involve the pericentromere of 16q. We present evidence from RNA-seq data that select genes, including SHCBP1, ORC6 and MYLK3, which are immediately downstream from the 16q pericentromere show heightened expression in MCF-7 cell line compared to the control. Data published by The Cancer Genome Atlas showed that all three genes have increased expression in breast tumor samples. We suggest that these genes are potential oncogenes for breast cancer progression. The search for tumor suppressor loss that accompanies the 16q loss ought to be augmented by the identification of potential oncogenes that gained expression during chromosomal rearrangements.
2022-07-12 | GSE207696 | GEO
Project description:Cancer genomes are characterized by accumulation of small-scale somatic mutations as well as large-scale chromosomal deletions, amplifications, and complex structural rearrangements. This characteristic is at least partially dependent on the ability of cancer cells to undergo recurrent chromosome breakage. In order to address to what extent chromosomal structural rearrangement breakpoints correlate with recurrent DNA double strand breaks (DSBs), we simultaneously mapped chromosome structural variation breakpoints by whole genome DNA-seq and spontaneous DSB formation by Break-seq in the breast cancer cell line MCF-7 and a non-cancer control cell line MCF-10A. We identified concurrent DSBs and structural variation breakpoints almost exclusively in the pericentromeric region of chromosome 16q in MCF-7 cells. We fine-tuned the identification of copy number variation breakpoints on 16q. In addition, we detected recurrent DSBs that occurred in both MCF-7 and MCF-10A. We propose a model for DSB-driven chromosome rearrangements that led to the translocation of 16q, likely with 10q, and the eventual 16q loss that does not involve the pericentromere of 16q. We present evidence from RNA-seq data that select genes, including SHCBP1, ORC6 and MYLK3, which are immediately downstream from the 16q pericentromere show heightened expression in MCF-7 cell line compared to the control. Data published by The Cancer Genome Atlas showed that all three genes have increased expression in breast tumor samples. We suggest that these genes are potential oncogenes for breast cancer progression. The search for tumor suppressor loss that accompanies the 16q loss ought to be augmented by the identification of potential oncogenes that gained expression during chromosomal rearrangements.
2022-07-12 | GSE207714 | GEO
Project description:Cancer genomes are characterized by accumulation of small-scale somatic mutations as well as large-scale chromosomal deletions, amplifications, and complex structural rearrangements. This characteristic is at least partially dependent on the ability of cancer cells to undergo recurrent chromosome breakage. In order to address to what extent chromosomal structural rearrangement breakpoints correlate with recurrent DNA double strand breaks (DSBs), we simultaneously mapped chromosome structural variation breakpoints by whole genome DNA-seq and spontaneous DSB formation by Break-seq in the breast cancer cell line MCF-7 and a non-cancer control cell line MCF-10A. We identified concurrent DSBs and structural variation breakpoints almost exclusively in the pericentromeric region of chromosome 16q in MCF-7 cells. We fine-tuned the identification of copy number variation breakpoints on 16q. In addition, we detected recurrent DSBs that occurred in both MCF-7 and MCF-10A. We propose a model for DSB-driven chromosome rearrangements that led to the translocation of 16q, likely with 10q, and the eventual 16q loss that does not involve the pericentromere of 16q. We present evidence from RNA-seq data that select genes, including SHCBP1, ORC6 and MYLK3, which are immediately downstream from the 16q pericentromere show heightened expression in MCF-7 cell line compared to the control. Data published by The Cancer Genome Atlas showed that all three genes have increased expression in breast tumor samples. We suggest that these genes are potential oncogenes for breast cancer progression. The search for tumor suppressor loss that accompanies the 16q loss ought to be augmented by the identification of potential oncogenes that gained expression during chromosomal rearrangements.
2022-07-12 | GSE207697 | GEO