Project description:CADM1, an immunoglobulin superfamily member, frequently inactivated but function as a tumor suppressor in many solid tumors. However, how CADM1 expression in ovarian cancer cells and the mechanisms of its tumor suppressor function is not fully understood. We created ovarian cancer ES-2 cell lines in which CADM1 was stably up-regulated. Genes differentially expressed in CADM1-overexpressing ES-2 cells.
Project description:Overexpression of transcription factor Sox17 in human ES cells-derived endothelial cells and hematopoietic cells enhances expansion of hemogenic endothelium-like cells.
Project description:In chimera assays, murine naïve embryonic stem (ES) cells usually produce better chimeras than the more primed epiblast-derived stem (EpiS) cells. Overexpression of the cytoskeleton-associated protein LIMA1/EPLIN in EpiS cells improves the rate of successful chimeras, while the knockout of LIMA1 in ES cells results in a metabolic state reminiscent of EpiS cells. To investigate the effects of LIMA1 we performed RNA-seq in Lima1 loss-of-function murine ES cells and in Lima1 gain-of-function murine EpiS cells and human induced pluripotent stem cells.
Project description:RNA-seq of murine ES cells with Lima1 knockout, murine EpiS cells with Lima1 overexpression and human iPS cells with LIMA1 overexpression
Project description:miRNA abnormalities are increasingly relevent to cancer development, We used microarrays to detail the global programme of gene expression upon miR-483 overexpression in sarcoma cell line MHH-ES-1.
Project description:Empty vector, SRF-dM-VP16 (control construct lacking the SRF DNA binding domain), or SRF-VP16 were expressed in wild-type ES cells (E14wt), SRF heterozygotes (E99-/+) or two SRF ko cell lines (E81-/-,E100-/-). RNA was harvested 72h after transfection. Each condition was performed in duplicate, except E100-/- vector transfected. Keywords: ordered
Project description:Genome editing research of human ES/iPS cells has been accelerated by clustered regularly interspaced short palindromic repeats/CRISPR-associated 9 (CRISPR/Cas9) and transcription activator-like effector nucleases (TALEN) technologies. However, the efficiency of biallelic genetic engineering in transcriptionally inactive genes is still low, unlike that in transcriptionally active genes. To enhance the biallelic homologous recombination efficiency in human ES/iPS cells, we performed screenings of accessorial genes and compounds. We found that RAD51 overexpression and valproic acid treatment enhanced biallelic-targeting efficiency in human ES/iPS cells regardless of the transcriptional activity of the targeted locus. Importantly, RAD51 overexpression and valproic acid treatment synergistically increased the biallelic homologous recombination efficiency. Our findings would facilitate genome editing study using human ES/iPS cells.
Project description:Overexpression of transcription factor Sox17 in human ES cells-derived endothelial cells enhances expansion of hemogenic endothelium-like cells.
Project description:The Polycomb group (PcG) gene products mediate heritable silencing of developmental regulators in metazoans, participating in one of two distinct multimeric protein complexes, the Polycomb repressive complexes-1 (PRC1) and -2 (PRC2)1. PRC2 catalyses trimethylation of histone H3 at lysine 27 (H3K27) which in turn is thought to provide a recruitment site for PRC1. Recent studies demonstrate that mono-ubiquitylation of histone H2A at lysine 119 is important in PcG mediated silencing with the core PRC1 component Ring1A/B functioning as the E3 ligase8. PRC2 has been shown to share target genes with the core transcription network to maintain embryonic stem (ES) cells including Oct4 and Nanog9. Here we identify an essential role for PRC1 in repressing developmental regulators in ES cells, and thereby in maintaining ES cell pluripotency. A significant proportion of the PRC1 target genes are also repressed by Oct4. We demonstrate that engagement of PRC1 and PRC2 at target genes is Oct4-dependent and moreover that Ring1B interacts with Oct4. Collectively these results show that PcG complexes are instrumental in Oct4-dependent repression required to maintain pluripotency of ES cells. This study provides a first functional link between a core ES cell regulator and global epigenetic regulation of the genome. Keywords: genetic modification
