The study entails novel bio-marker discovery of Tumor Aggressive Grade signature (TAGs) genes and their role in recurrence free survival of breast cancer (BC) patients. Current BC dataset was used for co-expression analysis of TAGs genes and their role in BC progression. Additionally, recent findings have suggested an importance of structural organization of sense-antisense gene pairs (SAGPs) for transcription, post-transcriptional and post-translational events and their associations with cancer and disease. We studied SAGPs in which both gene partners are protein encoding genes (coding-coding SAGPs), their role in human BC development and demonstrated their potential for BC stratification and prognosis. Based on gene expression and correlation analyses we identified the robust set of breast cancer-relevant SAGPs (BCR-SAGPs). We isolated and characterized the sense-antisense gene signature (SAGS) and evaluated its prognostic potential in various gene expression datasets comprising 1161 BC patients. The methods used included the Cox proportional survival analysis, statistical analysis of clinicopathologic parameters and differential gene expression. The SAGS was effective in identification of BC patients with the most aggressive disease. Independently, we validated the SAGS using 58 RNA samples of breast cancer tumors purchased from OriGene Technologies (Rockville, MD).
Sense-antisense gene-pairs in breast cancer and associated pathological pathways.
Age, Disease, Disease stage
View SamplesDeletion of Hdac3 impaired DNA repair and greatly reduced chromatin compaction and heterochromatin content. Liver-specific deletion of Hdac3 culminated in hepatocellular carcinoma. The loss of genomic stability and the impaired response to DNA damage suggested that a high mutation rate stimulated the development of HCC. To begin to assess what pathways were involved in the formation of HCC, we performed gene expression analysis using cDNA microarrys.
Hdac3 is essential for the maintenance of chromatin structure and genome stability.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
DAZAP1 regulates the splicing of Crem, Crisp2 and Pot1a transcripts.
Specimen part
View SamplesDeleted in Azoospermia Associated Protein 1 (DAZAP1) is a ubiquitous RNA-binding protein that is highly expressed in the testis. It is a component of the hnRNP particles and shuttles between the nucleus and the cytoplasm. Mice expressing the DAZAP1-Fn mutant protein manifest both growth retardation and spermatogenic arrest before meiosis I. To elucidate the biological function(s) of DAZAP1 and to search for its natural RNA substrates, we compared the expression profiles of wild-type and Dazap1 mutant testes by cDNA microarrays.
DAZAP1 regulates the splicing of Crem, Crisp2 and Pot1a transcripts.
Specimen part
View SamplesResistance of Calu3 NSCLC cells to the cytotoxic nucleoside analog gemcitabine (2',2'-difluorodeoxycytidine) can be prevented as well as reversed by the rexinoid X receptor selective agonist bexarotene. This study was designed to investigate the changes in gene expression associated with gemcitabine resistance and its reversal by bexarotene. In addition to the parental Calu3 cells and the 10 cycles of treatment of the gemcitabine resistant Calu3 cells with vehicle or bexarotene, analogous treatment paradigms with gemcitabine alone as well as the combination of both compounds have been included as controls. (However, it has to be noted that in the combination treatment, cells that were re-sensitized by bexarotene have largely been removed from the culture before harvest due to the cytotoxic activity of gemcitabine.)
Bexarotene (LGD1069, Targretin), a selective retinoid X receptor agonist, prevents and reverses gemcitabine resistance in NSCLC cells by modulating gene amplification.
No sample metadata fields
View SamplesBiological effects of overexpression of miR-146b microRNAs in the A549 human lung cancer cell-line was studied. A549 cells were engineered to express the precursor RNA (pre-miR-146b) that generates the miR-146b microRNAs. Control cells were engineered using the same gene expression plasmid (pLemiR, Open Biosystems) but without the pre-miR-146b insert. The Trans-Lentiviral GIPZ packaging system (Open Biosystems) was used to generate stable transfectant populations of the engineered cells.
Overexpression of the lung cancer-prognostic miR-146b microRNAs has a minimal and negative effect on the malignant phenotype of A549 lung cancer cells.
Disease, Cell line
View SamplesWe used RNA-seq to interrogate prostate cancer specific gene fusions, alternative splicings, somatic mutations and novel transcripts. Overall design: We sequenced the transcriptome (polyA+) of 20 prostate cancer tumors and 10 matched normal tissues using Illumina GAII platform. Then we used bioinformatic approaches to identify prostate cancer specific aberrations which include gene fusion, alternative splicing, somatic mutation, etc.
Recurrent chimeric RNAs enriched in human prostate cancer identified by deep sequencing.
No sample metadata fields
View SamplesOCM-1A uveal melanoma cells were infected with lentivirus carrying shRNA expression constructs specific for BAP1 or GFP (control), and placed under selection for 6 days. RNA-seq was performed. Overall design: Samples represent three independent experiments treated with control or BAP1 shRNA
Transposase mapping identifies the genomic targets of BAP1 in uveal melanoma.
Specimen part, Cell line, Treatment, Subject, Time
View SamplesWe used a novel approach to study the acute effect of three physiologic stressors (active contractions, vibration, and systemic heat stress) in human skeletal muscle. Three hours after the completion of a dose of physiologic stress, we sampled the soleus (contraction and vibration) or vastus lateralis (heat) muscle and developed a unique gene expression signature for each stressor. We discovered repetitive active muscle contractions up regulated metabolic transcription factors NR4A3 (12.45 fold change), PGC-1 (5.46 fold change), and ABRA (5.98 fold change); and repressed MSTN (0.56 fold change). Heat stress repressed PGC-1 (0.74 fold change); while vibration induced FOXK2 (2.36 fold change). Vibration similarly caused a down regulation of MSTN (0.74 fold change), but to a lesser extent than active muscle contraction. Vibration induced FOXK2 while heat stress repressed PGC-1 (0.74 fold change) and ANKRD1 genes (0.51 fold change). These findings support a distinct gene regulation in response to heat stress, vibration, and muscle contractions. Understanding these responses may assist in developing regenerative rehabilitation interventions to improve muscle cell development, growth, and repair.
Distinct Skeletal Muscle Gene Regulation from Active Contraction, Passive Vibration, and Whole Body Heat Stress in Humans.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Distinct metabolic states govern skeletal muscle stem cell fates during prenatal and postnatal myogenesis.
Age, Specimen part
View Samples