Leukemic cell lines expression profile of OTX015 compared to JQ1 and DMSO controls
Ontology highlight
ABSTRACT: Gene signature determination of the effect of a new bromodomain inhibitor among a representative set of leukemic cell lines OTX015 vs. DMSO and JQ1 vs. DMSO
Project description:Menthol, a naturally occurring cooling compound of peppermint oil, induces an anti-proliferative activity in androgen-independent prostate cancer (AIPC). Previously, we found that menthol affects PC-3 cells viability through activating JNK but the mechanism is not fully clear. We thus studied that dysregulated cell cycle progression of PC-3 cells to menthol. We performed microarray experiments to obtain a global view of how menthol affects prostate cancer biology in gene expression profile. Our study demonstrated that menthol induced G2/M arrest by dysregulating PLK1 in the AICP cell model. Menthol was dissolved in ethanol as a vehicle at 0.1% working concentration and treated in PC-3 cells in triplicate Vehicle-treated PC-3 cells in triplicate were used as control.
Project description:Analysis of the effects of the HNF4? antagonist, BIM5078, at the gene expression level. Results provide important information on the global effects of HNF4? antagonism on human gene expression in a cell line derived from human fetal islets. RNA was isolated from T6PNE cells subjected to 48 hours of treatment with either DMSO or BIM5078.
Project description:RNAseq is performed (50bp single end reads) on SW480, HT-29, HCT-15, HCT-116, COLO 205, and COLO 320 cell lines after DMSO or JQ1 treatment
Project description:Genome wide DNA methylation profiling of four female lymphoblastoid cell lines treated with DMSO control for 250 nM JQ1. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 485,000 CpGs.
Project description:T84 cells were treated with DMSO, 30nM trametinib (MEKi), 1µM JQ1 (BRD4i) or the combination of trametinib and JQ1 (combo) for 24h.
Project description:Gene Expression Microarray technology was used to compare oviduct transcriptome between inseminated and non-inseminated pigs during spontaneous oestrus. We used an in vivo model approaching the study from a physiological point of view in which no hormonal treatment (animals were in natural oestrus) and no artificial sperm selection (selection was performed within the female genital) were imposed. It is therefore emphasised that no surgical introduction of spermatozoa and no insemination at a site other than the physiological one were used. This approach revealed 17 genes that were two-fold or more up-regulated in oviducts exposed to spermatozoa and/or developing embryos and 9 genes that were two-fold or more down-regulated. These changes would indicate a modification of the environment preparing the oviduct for a successful fertilization and for an adequate embryo early development. The objective of this study was to investigate differences in oviductal transcriptome between inseminated and non-inseminated pigs during spontaneous oestrus in a specific area of the oviduct (ampullary-isthmic junction). We decided to analyse this specific part of the oviduct where spermatozoa released from sperm reservoir arrive close to the time of ovulation because it is where fertilization and zygote formation occurs. We used 5 artificially inseminated and 5 non-inseminated pigs during spontaneous oestrus. Inseminations were performed with seminal doses at a concentration of 3 x 107 spermatozoa/ml. Complete oviductal tissue samples from the ampullary-isthmic junction (sample size >1cm including the end of the ampulla) were taken from each animal and immediately frozen in liquid nitrogen for mRNA extraction.
Project description:SKBR-3 or BT474m1 HER2+ breast cancer cells were treated with either DMSO, 300nM lapatinib, 300nM JQ1, or lapatinib and JQ1 in combination for 48h.
Project description:BET bromodomain inhibitors effectively kill several types of cancer cells. However, the underlying mechanism of BET inhibition resistance remains obscure. We sought to identify the gene expression change upon treatment of JQ1, a well-known BET inhibitor, in basal-like breast cancer cells. In this dataset, we used RNA-sequencing to characterize the mRNA expression profiles from DMSO and JQ1-treated MDA-MB-231 breast tumor cells.
Project description:Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites resulting in changes in the transcription of specific genes. We used microarray profiling to investigate the transcriptional changes induced by BET inhibitor JQ1 treatment in DV90 cells to identify the underlying changes of gene regulation that lead to JQ1 sensitivity. DV90 cells (JQ1 sensitive non-small cell lung cancer cell line) were treated with 135 nM (IC50) or 785 nM (IC90) of JQ1 for 4h and 24h. DMSO treated controls served as reference and at least four replicates per condition were collected. RNA was extracted and hybridized to Affymetrix HuGene-2.1ST microarrays to identify treatment induced transcriptional changes.
Project description:Background Understanding how obesity impacts human mammary adipose tissue (MAT) biology is crucial for deciphering its role in mammary epithelium during both physiological and pathophysiological processes, including breast cancer. Hypertrophic mammary adipocytes and Crown-like Structures are present in MAT of obese patients but whether these changes initiate a fibro-inflammatory response at the tissue level remains insufficiently explored. Objective We aimed to investigate the markers of adipose tissue dysfunction (immune cell infiltration, secretion pattern and fibrosis) in tumor-free MAT of obese versus lean patients Methods Tumor-free MAT were obtained from 61 lean and obese women who underwent mastectomy for breast cancer risk reduction or treatment. Immune and non-immune cell infiltration was determined using flow cytometry. Bulk transcriptomic was used to characterize the phenotype of CD206+ macrophages whose infiltration is increased in obese. Conditioned-medium were prepared from MAT to characterize their secretome and dose adipokines and cytokines by ELISA assay. The extra-cellular matrix (ECM) deposition was evaluated by Masson trichrome staining on cross-stained sections and 3D imaging of red picrosirius-stained tissues. Results We observed an increase in CD206+/HLA-DR+ macrophages in the stromal vascular fraction of MAT from obese patients compared to lean ones. Other immune cell infiltration and endothelial or adipose progenitor cell numbers were similar between groups. Bulk transcriptomics on CD206+ macrophages revealed a significant decrease in ECM component secretion and processing in obese samples. Additionally, no heightened secretion of pro-inflammatory cytokines or MCP-1 was noted in obese samples. ECM characterization indicated an absence of fibrosis, with obese MAT showing reduced collagen secretion and deposition compared to lean counterparts. Conclusions Obesity does not associate with inflammation or fibrosis in MAT, underscoring its unique behavior.