Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA284879 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cancer relapse after curative treatment is thought to originate from drug-tolerant and invisible cancer cell subpopulations. Using cancer cell colonies emerging in the presence of drugs (drug-tolerant colonies, DTCs), we found that the drug-tolerant properties of DTCs are lost through a reversible mechanism. To examine whether epigenetic regulation is responsible for the phenotypic changes in DTCs, we performed a genome-wide analysis for relative CpG methylation between the DTCs and untreated colonies derived from MKN45 by NimbleGen Human Meth 385K Prom Plus CpG Arrays. Global changes in the methylation levels were evident in a chromosomal location-dependent manner. The methylation status of the upstream regions of the transcription start sites of the pluripotency-inducing genes showed good agreement with the qRT-PCR data. These results suggest that reversible drug-tolerant properties in DTCs are epigenetically regulated and associated with transcriptional regulation, including pluripotency-inducing factors. Comparison of untreated colonies v.s. DTCs derived from MKN45 cells.
2015-05-26 | E-GEOD-69203 | biostudies-arrayexpress
Project description:Transcriptional profiling of drug-tolerant cancer cell subpopulations
| PRJNA273955 | ENA
Project description:Cancer relapse after curative treatment is thought to originate from drug-tolerant and invisible cancer cell subpopulations. Using cancer cell colonies emerging in the presence of drugs (drug-tolerant colonies, DTCs), we found that the drug-tolerant properties of DTCs are lost through a reversible mechanism. To examine whether epigenetic regulation is responsible for the phenotypic changes in DTCs, we performed a genome-wide analysis for relative CpG methylation between the DTCs and untreated colonies derived from MKN45 by NimbleGen Human Meth 385K Prom Plus CpG Arrays. Global changes in the methylation levels were evident in a chromosomal location-dependent manner. The methylation status of the upstream regions of the transcription start sites of the pluripotency-inducing genes showed good agreement with the qRT-PCR data. These results suggest that reversible drug-tolerant properties in DTCs are epigenetically regulated and associated with transcriptional regulation, including pluripotency-inducing factors.
2015-05-26 | GSE69203 | GEO
Project description:Genome-wide DNA methylation analysis of breast cancer
| PRJNA302431 | ENA
Project description:Targeted therapies require life-long treatment, as drug discontinuation invariably leads to tumor recurrence. Recurrence is thought to mainly be driven by minor subpopulations of drug tolerant persister (DTP) cells that survive the cytotoxic drug effect. In lung cancer, DTP studies have mainly been conducted using tumor cell line models.
2022-12-21 | GSE199716 | GEO
Project description:Genome-wide DNA Methylation Analysis Reveals Novel Targets for Drug Development in Mantle Cell Lymphoma
| PRJNA120777 | ENA
Project description:Acquisition of drug resistance remains a chief impediment to successful cancer therapy, and we previously described a transient drug-tolerant cancer cell population (DTPs) whose survival is in part dependent on the activities of the histone methyltransferases G9a/EHMT2 and EZH2, the latter being the catalytic component of the polycomb repressive complex 2 (PRC2). Here, we applied multiple proteomic techniques to better understand the role of these HMTs in the establishment of the DTP state. Proteome-wide comparisons of lysine methylation patterns revealed that DTPs have increased methylation on K116 of PRC member Jarid2, an event that helps stabilize and recruit PRC2 to chromatin. We also found that EZH2, in addition to methylating histone H3K27, also methylates G9a at K185, and that methylated G9a better recruits repressive complexes to chromatin; similar to complexes recruited by histone H3 methylated at K9. Finally, a detailed histone posttranslational modification (PTM) analysis shows that EZH2, either directly or through its ability to methylate G9a, alters H3K9 methylation in the specific context of H3 serine10 phosphorylation, and primarily in a cancer cell subpopulation that serves as DTP precursors. We also show that combinations of histone PTMs recruit a different set of complexes to chromatin, shedding light on the temporal mechanisms that contribute to drug tolerance.
2020-01-24 | MSV000084838 | MassIVE
Project description:Anti-cancer drug sensitive DNA methylation marker research
| PRJNA137719 | ENA
Project description:Genome-wide DNA methylation analysis of different cell types
| PRJNA301715 | ENA
Project description:DNA methylation analysis of breast cancer cell-lines
| PRJNA214937 | ENA