Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA386885 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptome analysis of RNA samples from riboflavin-depleted HEK293T cells. Riboflavin is an essential component of the human diet and its derivative cofactors have an established role in oxidative metabolism. Riboflavin deficiency has been linked with various human diseases. In this study, we have modelled riboflavin deficiency in HEK293T cell line, shown remarkable increase of cell proliferation. The aim of the present study is to develop a cell culture model of riboflavin depletion and analyze its molecular mechanism of acceleration cell proliferation. So, we used Affymetrix Human Transcriptome Array 2.0 to identify genes that were differentially expressed upon riboflavin-depleted HEK293T cells.
2017-05-16 | GSE98927 | GEO
Project description:Microarray analysis has been applied to the cell proliferation in a human colonic cel line, Caco-2. We have shown previously that a moderate riboflavin depletion around weaning has a profound impact on the structure and function of the small intestine of the rat, which is not reversible following riboflavin repletion. In this study we have modelled riboflavin deficiency in a human cell line, shown irreversible loss of cell viability associated with impaired mitosis and identified candidate effectors of riboflavin depletion in the cell. The aim of the present study is to develop a cell culture model of riboflavin depletion and analyse its behaviour using a using a combination of cell biology approaches including microarray analysis. A human colonic cell line, Caco-2, was grown in culture and treated to riboflavin depletion. Treated and untreated cells were collected at appropriate time points and isolated RNA subjected to microarray analysis.
2009-03-06 | E-GEOD-15132 | biostudies-arrayexpress
Project description:Microarray analysis has been applied to the cell proliferation in a human colonic cel line, Caco-2. We have shown previously that a moderate riboflavin depletion around weaning has a profound impact on the structure and function of the small intestine of the rat, which is not reversible following riboflavin repletion. In this study we have modelled riboflavin deficiency in a human cell line, shown irreversible loss of cell viability associated with impaired mitosis and identified candidate effectors of riboflavin depletion in the cell. The aim of the present study is to develop a cell culture model of riboflavin depletion and analyse its behaviour using a using a combination of cell biology approaches including microarray analysis.
2009-03-06 | GSE15132 | GEO
Project description:Protein kinase CK2 is a conserved serine/threonine kinase that participates in various cellular processes. Elevated nuclear expression of CK2α has been observed in human carcinomas, but mechanisms for its variable localization in cells are poorly understood. This study demonstrates a functional connection between nuclear CK2 and gene expression in relation to cell proliferation. Growth stimulation of quiescent human fibroblasts identified a pool of CK2 highly phosphorylated at serine 7 of the α subunit that translocated into the nucleus. This phosphorylation appeared essential for its nuclear localization and catalytic activity. Protein signatures associated with nuclear CK2 complexes revealed enrichment of transcription factors and chromatin remodelers that seemed unique during progression through G1 phase of the cell cycle. Chromatin immunoprecipitation-sequencing profiling demonstrated recruitment of CK2α to the active gene locus, more abundantly in late G1 phase than in early G1. Notably, we confirmed the presence of CK2α at transcriptional start sites of core histone genes, growth stimulus-associated genes, and ribosomal RNAs. This study suggests that nuclear CK2α complexes, uniquely constituted during cell cycle progression, are essential for cell proliferation, by activating histone genes, triggering ribosome biogenesis, and then synthesize the components necessary for cell division, specified in the nucleus and also in the nucleolus.
2023-10-22 | PXD040882 | JPOST Repository
Project description:Riboflavin depletion impairs cell proliferation in intestinal cells: Identification of mechanisms and consequences
| PRJNA114951 | ENA
Project description:Riboflavin deficiency regulates inflammation-associated genes in rat esophageal intraepithelial neoplasia
| PRJNA436162 | ENA
Project description:Transcriptome analysis of control and MALAT1 lncRNA-depleted RNA samples from human diploid lung fibroblasts [WI38] The long noncoding MALAT1 RNA is upregulated in cancer tissues and its elevated expression is associated with hyper-proliferation, but the underlying mechanism is poorly understood. We demonstrate that MALAT1 levels are regulated during normal cell cycle progression. Genome-wide transcriptome analyses in normal human diploid fibroblasts reveal that MALAT1 modulates the expression of cell cycle genes, and is required for G1/S and mitotic progression. Depletion of MALAT1 leads to activation of p53 and its target genes. The cell cycle defects observed in MALAT1-depleted cells are sensitive to p53 levels, indicating that p53 is a major downstream mediator of MALAT1 activity. Furthermore, MALAT1-depleted cells display reduced expression of B-MYB (Mybl2), an oncogenic transcription factor involved in G2/M progression, due to altered binding of splicing factors on B-MYB pre-mRNA and aberrant alternative splicing. In human cells, MALAT1 promotes cellular proliferation by modulating the expression and/or pre-mRNA processing of cell cycle-regulated transcription factors. These findings provide mechanistic insights on the role of MALAT1 in regulating cellular proliferation. We analyzed RNA from control and MALAT1 depleted WI38 cells using the Affymetrix Human Exon 1.0 ST platform. Array data was analyzed by Partek Genomic Suite software.
2013-01-29 | E-GEOD-43830 | biostudies-arrayexpress
Project description:DEDD regulates cell cycle related genes
| PRJNA543152 | ENA
Project description:The long noncoding MALAT1 RNA is upregulated in cancer tissues and its elevated expression is associated with hyper-proliferation, but the underlying mechanism is poorly understood. We demonstrate that MALAT1 levels are regulated during normal cell cycle progression. Genome-wide transcriptome analyses in normal human diploid fibroblasts reveal that MALAT1 modulates the expression of cell cycle genes, and is required for G1/S and mitotic progression. Depletion of MALAT1 leads to activation of p53 and its target genes. The cell cycle defects observed in MALAT1-depleted cells are sensitive to p53 levels, indicating that p53 is a major downstream mediator of MALAT1 activity. Furthermore, MALAT1-depleted cells display reduced expression of B-MYB (Mybl2), an oncogenic transcription factor involved in G2/M progression, due to altered binding of splicing factors on B-MYB pre-mRNA and aberrant alternative splicing. In human cells, MALAT1 promotes cellular proliferation by modulating the expression and/or premRNA processing of cell cycle-regulated transcription factors. These findings provide mechanistic insights on the role of MALAT1 in regulating cellular proliferation. Keywords: MALAT1; MALAT-1, NEAT2, ncRNA; E2F, alternative splicing; pre-mRNA splicing factors WI38 cells (normal human diploid fibroblasts) were transfected with a control oligo (CTR) or antisense oligos to MALAT1 and RNA was isolated after 48 hr. Two antisense oligos were use for MALAT1 (AS-1 and AS-2). Arrays were done for 3 sets of samples in triplicate (control, AS-1 and AS-2).
2014-05-16 | E-GEOD-44240 | biostudies-arrayexpress