Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA134157 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Resveratrol induces downregulation of DNA repair genes in MCF7 human breast cancer cells.
2025-01-24 | E-GEOD-25412 | ExpressionAtlas
Project description:Arsenic is reportedly a biphasic inorganic compound for its toxicity and anticancer effects in humans. Recent studies have shown that certain arsenic compounds including arsenic hexoxide_x000D_ (AS4O6; hereafter, AS6) induce programmed cell death and cell cycle arrest in human cancer cells and murine cancer models. However, the mechanisms by which AS6 suppresses cancer cells are incompletely understood. In this study, we show markedly differential effects of AS6 on cytotoxicity and gene expression in human mammary epithelial normal cells (HUMEC) and Michigan Cancer Foundation 7 (MCF7), a human mammary epithelial cancer cell line. AS6 selectively arrests cell growth and induces cell death in MCF7 cells without affecting the growth of HUMEC in a dose-dependent_x000D_ manner. AS6 alters the transcription of a large number of protein-coding genes in MCF7 cells, but much fewer genes in HUMEC. Importantly, we found that the cell proliferation, cell cycle, and DNA repair pathways are significantly suppressed whereas cellular stress response and apoptotic pathways_x000D_ increase in AS6-treated MCF7 cells. Together, we provide the first evidence of differential effects of AS6 on normal and cancerous breast epithelial cells, suggesting that AS6 at moderate concentrations induces cell cycle arrest and apoptosis through modulating genome-wide gene expression, leading to compromised DNA repair and increased genome instability selectively in human breast cancer cells
2021-02-17 | GSE157574 | GEO
Project description:The emergence of drug resistance remains a critical challenge in cancer treatment, significantly contributing to high mortality rates. Here, we investigate therapy-induced senescence (TIS) as a reversible escape mechanism of drug resistance in breast cancer cells. Using high-dose doxorubicin, we induced TIS in MCF7 and T47D breast cancer cell lines. scRNA sequencing revealed a unique transcriptomic profile for TIS cells, distinct from both parental and repopulated cells in every cell line, exposing a small subpopulation of TIS cells with the potential to escape senescence. Gene set enrichment analysis indicated significant downregulation of proliferation-related genes, downregulation of DNA repair pathways, and the upregulation of immune response related genes.
2025-05-07 | GSE280381 | GEO
Project description:Breast cancer is a worlwide health problem. One of the factors involved in carcinogenesis is diet. Several studies indicate that resveratrol, a polyphenol present in diet, has several antitumor properties. The purpose of the study is gain an insight of resveratrol effect in cancer by determining the gene expression profile of breast cancer cell lines treated with the compound. MCF7 cell lines were treated for a 48 hour period with two concentrations (150 and 250 uM) of resveratrol. 9 plates were used for each condition. The RNA obtained from 3 plates of the same condition was pooled, processed and hybridized to the Affymetrix Human Gene 1.0 ST array. The arrays were analyzed using Partek Genomics suite software-.
2011-07-31 | E-GEOD-25412 | biostudies-arrayexpress
Project description:The emergence of drug resistance remains a critical challenge in cancer treatment, significantly contributing to high mortality rates. Here, we investigate therapy-induced senescence (TIS) as a reversible escape mechanism of drug resistance in breast cancer cells. Using high-dose doxorubicin, we induced TIS in MCF7, T47D, MDA-MB-231 and Hs578T breast cancer cell lines. Bulk RNA sequencing revealed a unique transcriptomic profile in TIS cells, distinct from both parental and repopulated cells in every cell line, exposing a small subpopulation of TIS cells with the potential to escape senescence. Gene set enrichment analysis indicated significant downregulation of proliferation-related genes, downregulation of DNA repair pathways, and the upregulation of immune response related genes.
2025-05-07 | GSE287953 | GEO
Project description:The proteins from the Fanconi Anemia (FA) pathway of DNA repair maintain DNA replication fork integrity by preventing the unscheduled degradation of nascent DNA at regions of stalled replication forks. Here, we ask if the bacterial pathogen H. pylori exploits the fork stabilisation machinery to generate double stand breaks (DSBs) and genomic instability. Specifically, we study if the H. pylori virulence factor CagA generates host genomic DSBs through replication fork destabilisation and collapse. An inducible gastric cancer model was used to examine global CagA-dependent transcriptomic and proteomic alterations, using RNA sequencing and SILAC-based mass spectrometry, respectively. The transcriptional alterations were confirmed in gastric cancer cell lines infected with H. pylori. Functional analysis was performed using chromatin fractionation, pulsed-field gel electrophoresis (PFGE), and single molecule DNA replication/repair fiber assays. We found a core set of 31 DNA repair factors including the FA genes FANCI, FANCD2, BRCA1, and BRCA2 that were downregulated following CagA expression. H. pylori infection of gastric cancer cell lines showed downregulation of the aforementioned FA genes in a CagA-dependent manner. Consistent with FA pathway downregulation, chromatin purification studies revealed impaired levels of Rad51 but higher recruitment of the nuclease MRE11 on the chromatin of CagA-expressing cells, suggesting impaired fork protection. In line with the above data, fibre assays revealed higher fork degradation, lower fork speed, daughter strands gap accumulation, and impaired re-start of replication forks in the presence of CagA, indicating compromised genome stability. By downregulating the expression of key DNA repair genes such as FANCI, FANCD2, BRCA1, and BRCA2, H. pylori CagA compromises host replication fork stability and induces DNA DSBs through fork collapse. These data unveil an intriguing example of a bacterial virulence factor that induces genomic instability by interfering with the host replication fork stabilisation machinery.
2022-02-22 | PXD031168 | Pride
Project description:The identification of reliable biomarkers is imperative for enhancing early detection, prognosis, and treatment of breast cancer. This study investigates a human telomeric dimeric G-quadruplex (G4) model, Tel46, which has been functionalized on Controlled Pore Glass (CPG) support, as a novel tool for biomarker discovery. Tel46 closely mimics multimeric G4 structures found in telomeric overhangs. Utilizing the affinity purification-mass spectrometry (AP-MS) approach, we identified 93 nuclear proteins that interacted with Tel46 in MCF7 breast cancer cells. Functional enrichment analyses revealed that these proteins were linked to DNA replication, repair, and genome stability pathways, which are frequently altered in cancer. To further refine these findings, we integrated AP-MS data with quantitative proteomics, comparing MCF7 and non-tumorigenic MCF10a cells. This approach led to the identification of 27 Tel46 interactors that were overexpressed. The subsequent functional analyses of these proteins revealed their enrichment in DNA replication, damage repair, and genome maintenance pathways, emphasising their potential as cancer biomarkers. Conversely, the downregulated proteins were associated with basic cellular functions such as protein synthesis and cytoskeletal organisation. Subsequent bioinformatics analyses incorporating public cancer genomics and transcriptomics data identified 19 potential biomarkers, including MSH6, MSH2, ESRP1, and WDHD1, which were further linked to poor clinical outcomes in breast cancer subtypes. This study validates the use of Tel46-functionalized CPG as a novel tool for isolating cancer-related proteins and highlights the potential of telomeric G4-interacting proteins as biomarkers for breast cancer diagnosis and therapy. These findings provide a foundation for future research into G4-mediated molecular mechanisms in cancer.
2025-09-15 | PXD059597 | Pride
Project description:The identification of reliable biomarkers is imperative for enhancing early detection, prognosis, and treatment of breast cancer. This study investigates a human telomeric dimeric G-quadruplex (G4) model, Tel46, which has been functionalized on Controlled Pore Glass (CPG) support, as a novel tool for biomarker discovery. Tel46 closely mimics multimeric G4 structures found in telomeric overhangs. Utilizing the affinity purification-mass spectrometry (AP-MS) approach, we identified 93 nuclear proteins that interacted with Tel46 in MCF7 breast cancer cells. Functional enrichment analyses revealed that these proteins were linked to DNA replication, repair, and genome stability pathways, which are frequently altered in cancer. To further refine these findings, we integrated AP-MS data with quantitative proteomics, comparing MCF7 and non-tumorigenic MCF10a cells. This approach led to the identification of 27 Tel46 interactors that were overexpressed. The subsequent functional analyses of these proteins revealed their enrichment in DNA replication, damage repair, and genome maintenance pathways, emphasising their potential as cancer biomarkers. Conversely, the downregulated proteins were associated with basic cellular functions such as protein synthesis and cytoskeletal organisation. Subsequent bioinformatics analyses incorporating public cancer genomics and transcriptomics data identified 19 potential biomarkers, including MSH6, MSH2, ESRP1, and WDHD1, which were further linked to poor clinical outcomes in breast cancer subtypes. This study validates the use of Tel46-functionalized CPG as a novel tool for isolating cancer-related proteins and highlights the potential of telomeric G4-interacting proteins as biomarkers for breast cancer diagnosis and therapy. These findings provide a foundation for future research into G4-mediated molecular mechanisms in cancer.
2025-09-15 | PXD059593 | Pride
Project description:Intraoperative radiotherapy (IOERT) is a high radiation therapeutic technique which administers a single high dose of ionizing radiation (IR) immediately after surgical tumor removal in order to destroy the residual cancer cells in the site at high risk for recurrence. IR is able to regulate several genes and factors involved in cell-cycle progression, survival and/or cell death, DNA repair and inflammation modulating an intracellular response radiation dependent producing an imbalance in cell fate decision. In this study, we examined changes in gene expression in MCF7 breast cancer cell line exposed to 9Gy and 23Gy high single dose of IR delivered by IOERT. Changes in gene expression in MCF7 breast cancer cell line exposed to 9Gy and 23Gy high single dose of IR (named MCF7_9Gy and MCF7_23Gy respectively), were analyzed as two-color hybridizations using Agilent Technologies whole human genome 4x44K microarrays
2015-06-11 | E-GEOD-63667 | 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