NPAS2 ChIP-on-chip in MCF7 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE15052 | GEO | 2009/03/07
SECONDARY ACCESSION(S): PRJNA114821
REPOSITORIES: GEO
Similar Datasets
Project description:Cancer cells have broken circadian clocks as compared to their normal tissue counterparts. Moreover, it has been shown in breast cancer that disruption of common circadian oscillations are associated to worse prognosis. Numerous studies focused at conical circadian genes in breast cancer cell lines have suggested that there are no mRNA circadian-like oscillations. Nevertheless, cancer cell lines have not been extensively characterized and it is unknown to what extent the circadian oscillations are disrupted. We have chosen representative breast cancer cell lines (MCF-10A, MCF-7, ZR-75-30, MDA-MB-231, and HCC-1954) in order to determine the degree which the circadian clock is damaged. We used serum shock to synchronize the circadian clocks in culture. Our aim was to observe the time course of gene expression using cDNA microarrays in the noncancerous MCF-10A and the cancerous MCF-7 cells and characterize specific genes in other cell lines. We used a cosine function to select highly correlated profiles. Some of the identified genes were validated by qPCR and further evaluated in the other breast cancer cell lines. Interestingly, we observed that breast cancer and noncancerous cultured cells are able to generate specific circadian expression profiles in response to the serum shock. The rhythmic genes suggested via microarray and measured in each particular subtype suggest that each breast cancer cell type respond differently to the circadian synchronization. Future results could identify circadian-like genes that are altered in breast cancer and noncancerous cells which can be used to propose novel treatments. Breast cell lines are potential models for in vitro studies of circadian clocks and clock-controlled pathways.
2016-04-01 | GSE76368 | GEO
Project description:Cancer cells have broken circadian clocks as compared to their normal tissue counterparts. Moreover, it has been shown in breast cancer that disruption of common circadian oscillations are associated to worse prognosis. Numerous studies focused at conical circadian genes in breast cancer cell lines have suggested that there are no mRNA circadian-like oscillations. Nevertheless, cancer cell lines have not been extensively characterized and it is unknown to what extent the circadian oscillations are disrupted. We have chosen representative breast cancer cell lines (MCF-10A, MCF-7, ZR-75-30, MDA-MB-231, and HCC-1954) in order to determine the degree which the circadian clock is damaged. We used serum shock to synchronize the circadian clocks in culture. Our aim was to observe the time course of gene expression using cDNA microarrays in the noncancerous MCF-10A and the cancerous MCF-7 cells and characterize specific genes in other cell lines. We used a cosine function to select highly correlated profiles. Some of the identified genes were validated by qPCR and further evaluated in the other breast cancer cell lines. Interestingly, we observed that breast cancer and noncancerous cultured cells are able to generate specific circadian expression profiles in response to the serum shock. The rhythmic genes suggested via microarray and measured in each particular subtype suggest that each breast cancer cell type respond differently to the circadian synchronization. Future results could identify circadian-like genes that are altered in breast cancer and noncancerous cells which can be used to propose novel treatments. Breast cell lines are potential models for in vitro studies of circadian clocks and clock-controlled pathways. There are 8 total samples representing 0 to 28 hours in 4 hour intervals in MFC-7 breast cancer epitheleal cell line.
2016-04-01 | E-GEOD-76368 | biostudies-arrayexpress
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2014-05-27 | GSE47041 | GEO
Project description:RNA-seq and ChIP-seq on MCF-7 breast cancer cell line upon activation of p53 by the non-genotoxic small molecule Nutlin-3a ChIP-seq on p53 in MCF7 with Nutlin-3a stimulation (S) in triplicate, and the control (input), in stimulated and non stimulated, using illumina HiSeq 2000
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2022-07-22 | GSE209080 | GEO
Project description:The individualized treatment of tumors has always been an urgent problem in clinical practice. Organoids-on-a-chip can reflect the heterogeneity of tumors and is a good model for in vitro anticancer drug screening. In this study, surgical specimens of patients with advanced colorectal cancer will be collected for organoid culture and organoids-on-a- chip. Use organoids-on-a-chip to screen tumor chemotherapy drugs, compare the results of patients’ actual medication regimens, and study the guiding role of organoids in the formulation of precise tumor treatment plans. The investigators will compare the response of organoids to drugs in vitro with the patient’s response to actual chemotherapy and targeted drugs and explore the feasibility and accuracy of organoids-on-a-chip based drug screening for advanced colorectal cancer. The project will establish a screening platform for chemotherapeutic drugs and targeted drugs based on colorectal cancer organoids to quickly and accurately formulate personalized treatment plans for clinical patients.
| 2385953 | ecrin-mdr-crc
Project description:Cancer cells have broken circadian clocks as compared to their normal tissue counterparts. Moreover, it has been shown in breast cancer that disruption of common circadian oscillations are associated to worse prognosis. Numerous studies focused at conical circadian genes in breast cancer cell lines have suggested that there are no mRNA circadian-like oscillations. Nevertheless, cancer cell lines have not been extensively characterized and it is unknown to what extent the circadian oscillations are disrupted. We have chosen representative breast cancer cell lines (MCF-10A, MCF-7, ZR-75-30, MDA-MB-231, and HCC-1954) in order to determine the degree which the circadian clock is damaged. We used serum shock to synchronize the circadian clocks in culture. Our aim was to observe the time course of gene expression using cDNA microarrays in the noncancerous MCF-10A and the cancerous MCF-7 cells and characterize specific genes in other cell lines. We used a cosine function to select highly correlated profiles. Some of the identified genes were validated by qPCR and further evaluated in the other breast cancer cell lines. Interestingly, we observed that breast cancer and noncancerous cultured cells are able to generate specific circadian expression profiles in response to the serum shock. The rhythmic genes suggested via microarray and measured in each particular subtype suggest that each breast cancer cell type respond differently to the circadian synchronization. Future results could identify circadian-like genes that are altered in breast cancer and noncancerous cells which can be used to propose novel treatments. Breast cell lines are potential models for in vitro studies of circadian clocks and clock-controlled pathways.
2016-04-01 | GSE76369 | GEO
Project description:Cancer cells have broken circadian clocks as compared to their normal tissue counterparts. Moreover, it has been shown in breast cancer that disruption of common circadian oscillations are associated to worse prognosis. Numerous studies focused at conical circadian genes in breast cancer cell lines have suggested that there are no mRNA circadian-like oscillations. Nevertheless, cancer cell lines have not been extensively characterized and it is unknown to what extent the circadian oscillations are disrupted. We have chosen representative breast cancer cell lines (MCF-10A, MCF-7, ZR-75-30, MDA-MB-231, and HCC-1954) in order to determine the degree which the circadian clock is damaged. We used serum shock to synchronize the circadian clocks in culture. Our aim was to observe the time course of gene expression using cDNA microarrays in the noncancerous MCF-10A and the cancerous MCF-7 cells and characterize specific genes in other cell lines. We used a cosine function to select highly correlated profiles. Some of the identified genes were validated by qPCR and further evaluated in the other breast cancer cell lines. Interestingly, we observed that breast cancer and noncancerous cultured cells are able to generate specific circadian expression profiles in response to the serum shock. The rhythmic genes suggested via microarray and measured in each particular subtype suggest that each breast cancer cell type respond differently to the circadian synchronization. Future results could identify circadian-like genes that are altered in breast cancer and noncancerous cells which can be used to propose novel treatments. Breast cell lines are potential models for in vitro studies of circadian clocks and clock-controlled pathways. There are 8 total samples representing 0 to 28 hours in 4 hour intervals in MFC-10A breast noncancerous epitheleal cell line.
2016-04-01 | E-GEOD-76369 | biostudies-arrayexpress
Project description:Proteotoxicity from insufficient clearance of misfolded/damaged proteins underlies many diseases. Carboxyl terminus of Hsc70-interacting protein (CHIP) is an important regulator of proteostasis in many cells, having E3-ligase and chaperone functions and often directing damaged proteins towards proteasome recycling. While enhancing CHIP functionality has broad therapeutic potential, prior efforts have all relied on genetic upregulation. Here we demonstrate that CHIP-mediated protein turnover is markedly post-translationally enhanced by direct protein kinase G (PKG) phosphorylation at S20 (mouse, S19 human). This increases CHIP binding affinity to Hsc70, CHIP protein halflife, and consequent clearance of stress-induced ubiquitinated-insoluble proteins. PKGmediated CHIP-pS20 or expressing CHIP-S20E (phosphomimetic) reduces ischemic proteo- and cytotoxicity, whereas a phospho-silenced CHIP-S20A amplifies both. In vivo, depressing PKG activity lowers CHIP-S20 phosphorylation and protein, exacerbating proteotoxicity and heart dysfunction after ischemic injury. CHIP-S20E knock-in mice better clear ubiquitinated proteins and are cardio-protected. PKG activation provides post-translational enhancement of protein quality control via CHIP.
2021-09-09 | PXD021531 | Pride