Parvin-beta is a focal adhesion protein downregulated in human breast cancer cells. Loss of Parvin-beta contributes to increased integrin-linked kinase activity, cell-matrix adhesion, and invasion through the extracellular matrix in vitro. The effect of ectopic Parvin-beta expression on the transcriptional profile of MDA-MB-231 breast cancer cells, which normally do not express Parvin-beta was evaluated. Particular emphasis was placed upon propagating MDA-MB-231 breast cancer cells in three-dimensional culture matrices. Gene expression profiles of vector control and Parvin-beta transfected MDA-MB-231 cells cultured on (A) monomeric type I collagen coated plastic, (B) embedded in a type I collagen gel, and (C) embedded in basement membrane (growth factor reduced Matrigel), were compared. Interestingly, Parvin-beta re-expression in MDA-MB-231 cells increased the mRNA expression, serine 82 phosphorylation (mediated by CDK9), and activity of the nuclear hormone receptor, peroxisome proliferator-activated receptor gamma (PPARgamma) and a concomitant increase in lipogenic gene expression as a downstream effector of PPARgamma. Importantly, Parvin-beta suppressed breast cancer growth in vivo with associated decreased proliferation. These data suggest that Parvin-beta might influence breast cancer progression..
Parvin-beta inhibits breast cancer tumorigenicity and promotes CDK9-mediated peroxisome proliferator-activated receptor gamma 1 phosphorylation.
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View SamplesColorectal cancer is one of the most common cancers in the world. Histological staging is efficient but combination with molecular markers may improve tumors classification. Gene expression profiles have been defined as prognosis predictors among stage II and III tumors but their implementation in medical practice remains controversial. Stage-II tumors have been recognized as a heterogeneous group and high-risk morphologic features have been retained as justifying adjuvant chemotherapy. We propose here the investigation of clinical features and expression profiles from stage II and stage III colon carcinomas without DNA mismatch repair defect. A series of 130 colon cancer samples was retained. Expression profiles were established on oligonucleotide microarrays and processed in the R/Bioconductor environment. Hierarchical then supervised analyses were successively performed applying the data-sampling approach. A molecular signature of seven genes was found to cluster stage III tumors with an adjusted p-values lower than 10^-10. A subgroup of stage-II tumors aggregated this cluster in both series. No correlation was found between with the disease severity but the function of the discriminating genes suggests that tumors have been classified according to their putative response to adjuvant targeted or classic therapies. Further pharmacogenetic studies might document this observation.
A seven-gene signature aggregates a subgroup of stage II colon cancers with stage III.
Sex, Age, Specimen part
View SamplesAnalysis of expression profiles in stage II colon cancer according to the APC gene status
Expression Profiles in Stage II Colon Cancer According to APC Gene Status.
Sex, Age, Specimen part
View SamplesThe aim of this study was to assess the impact of oocyte competence on subsequent fertility. Based on knowledge already accessible in mammals and on bioinformatics tools including the chicken genome sequence, we focused on the expression of genes involved in the processes of fertilization and of early embryo development.
Search for the genes involved in oocyte maturation and early embryo development in the hen.
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View SamplesPlant immune responses to pathogen attack involve various defense mechanisms and among them, the Hypersensitive Response (HR), a form of programmed cell death occurring at invasion sites. AtMYB30, a transcription factor acts as a positive regulator of a cell death pathway conditioning the HR.
A MYB transcription factor regulates very-long-chain fatty acid biosynthesis for activation of the hypersensitive cell death response in Arabidopsis.
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View SamplesBio-electrospray, the direct jet-based cell handling apporach, is able to handle a wide range of cells. Studies at the genomic, genetic, and the physiological level have shown that, post-treatment, cellular integrity is unperturbed and a high percentage (>70%, compared to control) of cells remain viable. Although, these results are impressive, it may be argued that cell based systems are oversimplistic. This study utilizing a well characterised multicellular model organism, the non-parasitic nematode Caenorhabditis elegans. Nematodes were subjected to bio-electrosprays to demonstrate that bio-electrosprays can be safely applied to nematodes.
Bio-electrospraying the nematode Caenorhabditis elegans: studying whole-genome transcriptional responses and key life cycle parameters.
Specimen part
View SamplesTo evaluate gene expression changes in mixed tissue samples used as process controls in male Sprague Dawley rats over time.
Assessment of repeated microarray experiments using mixed tissue RNA reference samples.
No sample metadata fields
View SamplesOriginal patient tumor is directly implanted in mice xenografts. Tumor is propagated to multiple mice for conduct of 6 arm treatment trials and control. Therapies are selected based on T0 and F0 genomic profiles.
Using a rhabdomyosarcoma patient-derived xenograft to examine precision medicine approaches and model acquired resistance.
No sample metadata fields
View SamplesUterine double conditional inactivation of Smad2 and Smad3 in mice results in endometrial dysregulation, infertility, and uterine cancer. Smad2/3 cKO mice demonstrate abnormal expression of genes involved in inflammation, cell-cycle checkpoint, migration, steroid biosynthesis, and SMAD1/5-driven genes. We performed RNA-sequencing to identify the gene expression differences between the uterine epithelium of control and Smad2/3 cKO. To control for estrous cycle variations, the uterine epithelium was collected from mice at 0.5 dpc. Global gene expression profiles of Smad2/3 cKO versus control mice was analyzed. Our RNA sequencing analysis was performed at 6 weeks of life and already showed significant differences in migratory (Agr2,Slit2) and inflammatory (Ccl20, Crispld2) markers between Smad2/3 cKO and control mice. Overall design: Two group comparison: uterine epithelium of control and Smad2/3 cKO mice. We generated a conditional knockout of Smad2/3 in the uterus and demonstrated that Smad2/3 plays a critical role in the endometrium, with disruption resulting in pubertal-onset uterine hyperplasia and ultimately fatal uterine cancer.
Uterine double-conditional inactivation of <i>Smad2</i> and <i>Smad3</i> in mice causes endometrial dysregulation, infertility, and uterine cancer.
Specimen part, Subject
View Samplessorafenib is the treatment of reference for hepatocellular carcinoma (HCC). We applied sorafenib on the human HCC cell line Huh7 and the subclone shRb, carrying a stable knock-down of the expression of the RB1 gene, a key regulator of liver carcinogenesis. Our aim was to better understand the physiologic and metabolic consequences of the exposure of HCC cells to sorafenib.
Metallothionein-1 as a biomarker of altered redox metabolism in hepatocellular carcinoma cells exposed to sorafenib.
Specimen part, Cell line, Treatment
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