Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-7578
PROVIDER: PRJNA100319 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcription profiling by array of human medulloblastoma cells after knock-down of Bmi-1 and Mel-18
2025-01-24 | E-GEOD-7578 | ExpressionAtlas
Project description:Bmi-1 and Mel-18 are close structural homologues that belong to the polycomb group (PcG) of transcriptional regulators of homeotic gene expression in development. They are believed to stably maintain repression of gene expression by altering the state of chromatin at specific promoters. A number of clinical and experimental observations have also implicated Bmi-1 in tumorigenesis and stem cell maintenance. Bmi-1 overexpression or amplification has been observed in a number of human malignancies, particularly in B-cell lymphomas, medulloblastomas and breast cancer. We report here that shRNA-mediated knock-down of either Bmi-1 or Mel-18 in human medulloblastoma DAOY cells results in the inhibition of proliferation, loss of clonogenic survival and anchorage-independent growth, and suppression of xenograft tumor formation in nude mice. Furthermore, overexpression of both Bmi-1 and Mel-18 significantly increased clonogenic survival of Rat1 fibroblasts. In contrast, stable downregulation of Bmi-1 or Mel-18 alone did not affect the growth of SK-OV-3 or U2OS cancer cell lines or normal human WI38 fibroblasts. Gene expression analysis of shRNA-expressing DAOY cells has demonstrated a significant overlap in the Bmi-1- and Mel-18-regulated genes and revealed novel gene targets under their control. Taken together, these results suggest that Bmi-1 and Mel-18 might have overlapping functions in human tumorigenesis. Keywords: shRNA knock-down
2007-05-01 | GSE7578 | GEO
Project description:Bmi-1 and Mel-18 are close structural homologues that belong to the polycomb group (PcG) of transcriptional regulators of homeotic gene expression in development. They are believed to stably maintain repression of gene expression by altering the state of chromatin at specific promoters. A number of clinical and experimental observations have also implicated Bmi-1 in tumorigenesis and stem cell maintenance. Bmi-1 overexpression or amplification has been observed in a number of human malignancies, particularly in B-cell lymphomas, medulloblastomas and breast cancer. We report here that shRNA-mediated knock-down of either Bmi-1 or Mel-18 in human medulloblastoma DAOY cells results in the inhibition of proliferation, loss of clonogenic survival and anchorage-independent growth, and suppression of xenograft tumor formation in nude mice. Furthermore, overexpression of both Bmi-1 and Mel-18 significantly increased clonogenic survival of Rat1 fibroblasts. In contrast, stable downregulation of Bmi-1 or Mel-18 alone did not affect the growth of SK-OV-3 or U2OS cancer cell lines or normal human WI38 fibroblasts. Gene expression analysis of shRNA-expressing DAOY cells has demonstrated a significant overlap in the Bmi-1- and Mel-18-regulated genes and revealed novel gene targets under their control. Taken together, these results suggest that Bmi-1 and Mel-18 might have overlapping functions in human tumorigenesis. Experiment Overall Design: DAOY cells were transduced with the indicated lentiviral shRNA and stable cell lines were generated by selection in puromycin (1 µg/ml). 2 x 105 cells of each stable cell line were plated onto 60 mm dishes in triplicates and harvested 4 days later. Triplicate total RNA samples from shRNA-expressing and mock-transduced DAOY cells were isolated using affinity resin (Qiagen RNeasy Mini Kit, Qiagen AG). RNA Integrity and purity were assessed with the RNA 6000 Nano LabChip system on Bioanalyzer 2100 (Agilent Technologies). Gene array analysis was conducted at the Genomics Factory at Novartis PHARMA AG, Basel, Switzerland using Gene Chip Human Genome 133 2.0 Plus Expression Array (Affymetrix Inc.).
2007-10-31 | E-GEOD-7578 | biostudies-arrayexpress
Project description:Transcription profiling by array of human UKE-1 cells with shRNA mediated knock-down of ASXL1
2025-01-24 | E-GEOD-38692 | ExpressionAtlas
Project description:RNA-seq following shRNA-mediated knock-down of ETV6-RUNX1 in the B-ALL cell line Reh
2025-01-23 | E-MTAB-10308 | ExpressionAtlas
Project description:Genome-wide transcriptome profiling of SK-Mel-28, UACC-62 and HCT-116 cells stably expressing scrambled shRNA and RAB7 shRNA
2025-01-24 | E-GEOD-42735 | ExpressionAtlas
Project description:Transcription profiling by high throughput sequencing between ASCC3 knock-down cells and control cells
2025-01-24 | E-GEOD-47399 | ExpressionAtlas
Project description:shRNA mediated knock-down of Tal1 in human Endothelial Colony Forming Cells (ECFCs)
| PRJNA190045 | ENA
Project description:Effect on JNK knock-down in INS-1 insulin-producing cells
2014-12-05 | E-MTAB-3146 | ExpressionAtlas
Project description:MEL clone 745 cells that are blocked at the pro-erythroblast stage serve as a model for terminal erythroid differentiation when treated with DMSO. A stable MEL cell line expressing (Dox)-dependent shRNA sequence targeting different regions of G9a mRNA was established and screened as previously described in (Demers, 2007 PMID17707229). Knock down was induced by adding 5 micrograms/ml final of Dox in the culture medium. For a total of six samples, 10 micro grams of RNA was extracted from each three biological replicates of mouse erythroleukemia (MEL) cells and their corresponding G9a knock downs. The RNA was extracted and purified using the RNeasy Mini Kit (Qiagen) including the on-column DNAse I digestion step. Experiment Overall Design: Mouse erythroleukemia cells: wild type vs G9 knock down. For each microarray hybridization, data analysis was performed using MAS and GCRMA.
2009-11-09 | E-GEOD-15620 | biostudies-arrayexpress