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Human TNBC Cells 72h Treatment with 4.5nM OTSSP167 MELK Inhibitor vs. DMSO Control

ABSTRACT: Microarray comparing TNBC cells treated for 72 hours with OTSSP167 MELK Inhibitor and control (DMSO) Two-condition arrays: MDA-MB-231 cells were treated with either 4.5nM OTSSP167 MELK Inhibitor or 0.045% DMSO for 72h. Two biological replicates, one per array, with a dye swap (technical replicate).

ORGANISM(S): Homo sapiens

SUBMITTER: Cecilia Williams

PROVIDER: E-GEOD-68691 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide effects of MELK-inhibitor in triple-negative breast cancer cells indicate context-dependent response with p53 as a key determinant.

Simon Marisa M Mesmar Fahmi F Helguero Luisa L Williams Cecilia C

PloS one 20170224 2

Triple-negative breast cancer (TNBC) is an aggressive, highly recurrent breast cancer subtype, affecting approximately one-fifth of all breast cancer patients. Subpopulations of treatment-resistant cancer stem cells within the tumors are considered to contribute to disease recurrence. A potential druggable target for such cells is the maternal embryonic leucine-zipper kinase (MELK). MELK expression is upregulated in mammary stem cells and in undifferentiated cancers, where it correlates with poo ...[more]

PMID: 28235006

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Human TNBC Cells 72h Treatment with 4.5nM OTSSP167 MELK Inhibitor vs. DMSO Control (SUM159)

Project description:Microarray comparing TNBC cells treated for 72 hours with OTSSP167 MELK Inhibitor and control (DMSO) Two-condition arrays: SUM159 cells were treated with either 4.5nM OTSSP167 MELK Inhibitor or 0.045% DMSO for 72h. Two biological replicates, one per array, with a dye swap (technical replicate).

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Human TNBC Cells 72h Treatment with 45nM OTSSP167 MELK Inhibitor vs. DMSO Control (SUM159)

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Human TNBC Cells 48h Treatment with OTSSP167 MELK Inhibitor vs. DMSO Control

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Human Corneal Epithelial Cells (SV40-HCEC) 6h Treatment with 100nM Vitamin D (1,25D3) vs. Vehicle Control

Project description:Inflammatory signals must be regulated and kept in check in order to prevent tissue damage.Â This is especially true in the cornea, where damage can induce loss of transparency, essential for vision.Â Toll-like receptors (TLRs) are present at the ocular surface and, in addition to being protective against infection, have also been implicated in the pathogenesis of dry eye syndrome, an inflammatory condition that affects millions of individuals in the United States each year.Â Â Therefore, an important area of research is the development of new anti-inflammatory therapeutics that limit aberrant ocular surface inflammation.Â Vitamin D has been studied for its role in suppressing inflammation in other tissues.Â In previous studies, we have demonstrated that vitamin D is able to decrease proinflammatory mediators induced by TLRs in human corneal epithelial cells (HCEC).Â Therefore, the goal of the current study was to examine this mechanism further through an evaluation of vitamin Dâ??s influence on gene expression in two different HCEC cell lines. Microarray comparing SV40-HCEC, human corneal epithelial cells, treated for 6 hours with Vitamin D (1,25D3) and control (0.1% ethanol) Two-condition arrays: SV40-HCEC cells were treated with either 100nM 1,25D3 or 0.1% Ethanol for 6h. Two biological replicates, one per array, with a dye swap (technical replicate).

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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Project description:Microarray comparing TNBC cells treated for 72 hours with OTSSP167 MELK Inhibitor and control (DMSO)

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Project description:Microarray comparing TNBC cells treated for 72 hours with OTSSP167 MELK Inhibitor and control (DMSO)