Gene expression profiles in KRAS mutant A549 cells after BI-2536 and fasudil combination treatment
Ontology highlight
ABSTRACT: To identify the potential mechanisms of enhanced activity of combined inhibition of PLK1 and ROCK, we conducted a microarray analysis on gene expression profiles in KRAS mutant A549 cells. We used Affymetrix GeneChip PrimeView Human Gene Expression array to detail gene expression after indicated treatments and identified the molecular mechanism during this process to facilitate further studies. A549 cells were treated with vehicle control, BI-2536 (4 nM), fasudil (20 µM), or the combination of BI-2536 and fasudil for 6 h. Samples were obtained from three independent biological replicates.RNA from each sample was labeled and hybridized using Affymetrix GeneChip PrimeView Human Gene Expression array.
Project description:To identify the potential mechanisms of enhanced activity of combined inhibition of PLK1 and ROCK, we conducted a microarray analysis on gene expression profiles in KRAS mutant A549 cells. We used Affymetrix GeneChip PrimeView Human Gene Expression array to detail gene expression after indicated treatments and identified the molecular mechanism during this process to facilitate further studies.
Project description:Bi-sex male and female Schistosoma mansoni worms were isolated from mice 7-weeks post-infection. Bi-sex male material or female material was compared in a direct bimodal comparison to single-sex male or female material. Two independent biological batches of both bi- and single-sex males were used. One batch of single-sex female material was used in comparisons to three independent biological batches of bi-sex female material. A dye-swap hybridization was performed for each bimodal comparisons in turn.
Project description:This microarray experiment was designed to identify genes and pathways modulated in ovarian cancer xenografts treated with anti-human VEGF mAb (Bevacizumab). Tumors were established in NOD/SCID mice by s.c. injection of human ovarian cancer cells (IGROV-1 and SKOV3). Mice were treated with the anti-VEGF monoclonal antibody Bevacizumab or with PBS (control). Total RNA was extracted from tumor samples and hybridized on Affymetrix GeneChip™ PrimeView™ Human Gene Expression Arrays. Each sample was derived from a different mouse (n=5 mice/group). In order to evaluate the effects of the anti-human VEGF mAb in the two models, expression data of IGROV-1 and SKOV3 derived tumors were normalized and analyzed separately. Raw microarray data, preprocessed data matrix and results of differential expression analysis are available together with the applied protocols.
Project description:GeneChip PrimeView Human PathArrayTM was performed using the SiHa cells-stably expressing shCtrl or shSYT7. To investigate the underlying mechanism of tumor-suppressive phenotypes of CESC with SYT7 knockdown, we used GeneChip PrimeView Gene Expression Array that could detect expression profiling of over 36,000 transcripts and variants using the SiHa-shCtrl and shSYT7-cDNAs
Project description:We used microarrays to detail the global programme of gene expression underlying Polo-like kinase inhibition with BI 2536 compound in mouse bone marrow-derived dendritic cells (BMDCs) stimulated with Toll-like receptor agonists LPS and poly(I:C). CD11c+ BMDCs were treated for 1 hour with BI 2536 (1µM) or vehicle control (DMSO) prior to stimulation with LPS or poly(I:C) for 4 h. Total RNA was extracted and prepared for hybridization on Affymetrix microarrays.
Project description:Genome wide expression profiling of ulcerative colitis, and normal colon mucosa samples. The GeneChip PrimeView Human Gene Expression Array was used to obtain expresion profiles across colon mucosa samples. Samples came from 5 ulcerative colitis affected, and 5 normal individuals.
Project description:The mechanisms regulating breast cancer differentiation state are poorly understood. Of particular interest are molecular regulators controlling the highly aggressive and poorly differentiated traits of basal-like breast carcinomas. Here we show that the Polycomb factor EZH2 maintains the differentiation state of basal-like breast cancer cells, and promotes the expression of progenitor-associated and basal-lineage genes. Specifically, EZH2 regulates the composition of basal-like breast cancer cell populations by promoting a M-bM-^@M-^\bi-lineageM-bM-^@M-^] differentiation state, in which cells co-express basal- and luminal-lineage markers. We show that human basal-like breast cancers contain a subpopulation of bi-lineage cells, and that EZH2-deficient cells give rise to tumors with a decreased proportion of such cells. Bi-lineage cells express genes that are active in normal luminal progenitors, and possess increased colony formation capacity, consistent with a primitive differentiation state. We found that GATA3, a driver of luminal differentiation, performs a function opposite to EZH2, acting to suppress bi-lineage identity and luminal progenitor gene expression. GATA3 levels increase upon EZH2 silencing, leading to the observed decrease in bi-lineage cell numbers. Our findings reveal a novel role for EZH2 in controlling basal-like breast cancer differentiation state and intra-tumoral cell composition. Total of four treatments (HCC70 cells stably expressing shEZH2, shEED, or EZH2 cDNA, and MDA-MB-468 cells stably expressing shEZH2) were done in duplicates, each with its own control.