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Differential gene expression in Ki-RAS and Ha-RAS cell lines.

ABSTRACT: Comparison of gene expression in Ha-RAS transformed cells versus untransformed Caco-2. Comparison of gene expression in Ki-RAS transformed cells versus untransformed Caco-2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE12203 | GEO | 2009/04/07

SECONDARY ACCESSION(S): PRJNA113431

REPOSITORIES: GEO

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Gene regulation in ki-ras transfected murine fibroblasts

Project description:Ki-ras gene mutations are involved in the carcinogenesis of acute myeloid leukemia, melanoma and different carcinomas. In order to define potential mutation-specific therapeutic targets, expression profiling analyses were performed using stable transfected NIH3T3 cells carrying different ki-ras gene mutations. Maybe, this analysis allows the discorvery of ras-associated cellular mechanisms, which might lead to the identification of physiological targets for pharmacological interventions of the treatment of Ki-ras-associated human tumors. Keywords: cDNA microarray, murine fibroblast, ki-ras mutations, carcinogenesis 4 transfected murine fibroblast cell lines (mock, wt-kras, Asp, Val) were compared to non-transfected cell line. For each of the four comparison 4 chip experiments were performed including 2 dye swaps.

2010-05-25 | E-GEOD-8372 | biostudies-arrayexpress

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Ki-67 organises heterochromatin during cell proliferation

Project description:Antigen Ki-67 is a nuclear protein expressed in proliferating mammalian cells. It is widely used in cancer histopathology but its functions remain unclear. Here, we show that Ki-67 controls heterochromatin organisation. Altering Ki-67 expression levels did not significantly affect cell proliferation in vivo. Ki-67 mutant mice developed normally and cells lacking Ki-67 proliferated efficiently. Conversely, upregulation of Ki-67 expression in differentiated tissues did not inhibit cell cycle arrest. Ki-67 interactors included proteins involved in nucleolar processes and chromatin regulators. Ki-67 depletion disrupted nucleologenesis but did not inhibit pre-rRNA processing. In contrast, it altered gene expression. Ki-67 silencing also had wide-ranging effects on chromatin organisation, disrupting heterochromatin compaction and long-range genomic interactions. Trimethylation of histone H3K9 and H4K20 at heterochromatin was strongly reduced. Overexpression of human or Xenopus Ki-67 induced ectopic heterochromatin formation. Altogether, our results suggest that Ki-67 expression in proliferating cells spatially organises heterochromatin, thereby controlling gene expression.

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