Project description:To investigate the effect of TMIGD2 on transcriptional functions in human AML cell line, we performed gene expression profiling analysis using data obtained from RNA-seq of HEL cells upon TMIGD2 knockdown.
Project description:compare the gene expression profile between cep701 treated HEL cells with shPRMT5 knockingdown HEL cells. HEL cells contain homologous alells with mutation Jak2V617F. We found JAK2V617F can inactivate PRMT5 activity by directly phosphorylating PRMT5 through histone methylation.
Project description:To understand the role of LSD1 in regulating histone H3K4 methylation status, ChIP-seq analyse of mono- and di-methylated H3K4 in LSD1-KD HEL cells were performed. The analyses revealed demethylation of H3K4me1 and H3K4me2 by LSD1 at regulatory regions including CEBPA gene enhancer.
Project description:This study aims to determine the chromosome content and organisation of two myeloid leukaemia cell lines, HEL and U937. This will be done not only with SNP array data to determine breakpoints and copy number of copy number aberrations, but also with FISH (multicolour FISH, multicolour banding, centromere and single locus FISH) to identify translocation partners, chromosome organistion, centromere content, and provide some information on genome evolution in the cell line. Although several HEL SNP array karyotypes have been published and are available online the information here shows that there are some differences, and the additional FISH tests provide a greater depth of information on genome organisation and derivation of the abnormal chromosomes. The U937 cell line was also studied using DNA from fresh and fixed specimens for comparison of the quality of the SNP array data. Data from cells fixed using standard cytogenetic fixative (3:1 methanol:acetic acid) were compared to data from cells processed directly from tissue culture.
2013-11-30 | GSE41964 | GEO
Project description:Whole human genome methylation analysis of the HEL cell line using nanopore sequencing
| PRJEB45078 | ENA
Project description:Whole human genome methylation analysis of the HEL cell line using nanopore sequencing
Project description:We used the nanopore Cas9 targeted sequencing (nCATS) strategy to specifically sequence 125 L1HS-containing loci in parallel and measure their DNA methylation levels using nanopore long-read sequencing. Each targeted locus is sequenced at high coverage (~45X) with unambiguously mapped reads spanning the entire L1 element, as well as its flanking sequences over several kilobases. The genome-wide profile of L1 methylation was also assessed by bs-ATLAS-seq in the same cell lines (E-MTAB-10895).
Project description:The mutant JAK2v617F is a driver of myeloproliferative neoplasms(MPNs). Consequently, several JAK2 inhibitors are currently being studied in clinical trials. The most investigated JAK2 inhibitor, Ruxolitinib, provides significant and sustained improvements in spleen related and constitutional symptoms secondary to the disease and represents a milestone in the treatment of myelofibrosis. However, JAK2 inhibitors are non-curative and murine experiments have shown that JAK2 inhibitors don?t eradicate MPN stem cells. In the present study, we determined the effect of the specific JAK2V617F inhibitor LY2784544 on leukemic stem (CD34+) cells (LSCs) using the JAK2V617F-bearing erythroleukemia cell line HEL. The LY2784544 treatment caused a transient proliferation inhibition and apoptosis of HEL cells, but a recovery occurred within a week. Thereafter, the continuous exposure of HEL cells to LY2784544 induced the accumulation of CD34+ LSCs, and the CD34+ cell fraction increased from 8% to over 90% by week 9, which was accompanied by substantially increased clonogenic potentials. A whole-transcript expression analysis revealed a significantly enhanced expression of the stem cell factor KLF4 in LY2784544 treated HEL cells. Inhibiting KLF4 expression attenuated LY2784544-mediated accumulation of CD34+ LSCs. Moreover, we further identified that the telomerase inhibitor GRN163L abolished the LY2784544-mediated CD34+ cell enrichment. Our findings collectively suggest that JAK2 inhibitors may cause enrichment of LSCs and are therefore unlikely to cure MPN as a monotherapy. Moreover, simultaneously targeting JAk2V617F and KLF4 or telomerase may be a novel strategy for MPN treatment.
