Chromosomal aberrations of human bladder cancer cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE19714 | GEO | 2010/01/05
SECONDARY ACCESSION(S): PRJNA121907
REPOSITORIES: GEO
Similar Datasets
Project description:Five bladder cancer (BC) cell lines were subjected to high-resolution array comparative genomic hybridization (CGH), which contained about 244,000 probes. The focus was on the typical gain locus of 8q24.3, which has not been studied in detail for BC. Integrating array-CGH data with the results of gene-expression profiling using oligo-microarray analysis revealed that 34 genes on 8q24.3 were generally up-regulated in the cell lines. Among these 34 genes, lymphocyte antigen 6 complex locus K (LY6K), which is a cancer/testis antigen, was the most up-regulated one in the BC (13.76-fold) as well as in clinical BC samples (2.84-fold). Investigation molecular network of LY6K performed using another oligo-microarray of the LY6K transfectant demonstrated that 269 genes were generally up-regulated more than five-fold in the transfectant. Twenty-one percent of the up-regulated genes were annotated into ‘cell cycle’ category, suggesting that LY6K is a promising molecular target for BC.
2010-01-05 | GSE19712 | GEO
Project description:Based on the identification of G9a as a potential target in BC, we decided to test the effect of a recently described dual inhibitor against G9a/DNMTs, CM-272, in several BC cell lines
2019-02-01 | GSE115544 | GEO
Project description:Prohibitin (PHB) plays a significant role in cancer processes whereas its mechanism in bladder cancer (BC) aggressiveness is not fully understood. This study aimed to investigate the role of PHB in BC aggressiveness. The study employed a range of in vivo and in vitro assays to elucidate the interaction between PHB-NADSYN1 and its underlying function in BC progression. We found that PHB was upregulated in muscle-invasive bladder cancer tissues, and bound to NADSYN1 mRNA in BC tissues more than in adjacent normal tissues. NADSYN1 and PHB were upregulated and positively correlated both in BC tissues and cell lines. We further revealed that deleting NADSYN1 prevented PHB-mediated cell invasiveness of BC in vivo and in vitro. PHB could directly bind to NADSYN1 mRNA, and it was found that the PHB domain was responsible for the PHB-NADSYN1 interaction. Depletion of NADSYN1 expression significantly decreased the protein level of PHB. In addition, Snai2 positively correlated with NADSYN1 and depletion or mutation of Snai2 binding sites inhibited NADSYN1-PHB-mediated BC progression. The study highlights a novel Snai2-NADSYN1-PHB mechanism in BC progression and indicates that PHB and NADSYN1 could serve as a therapeutic target for BC
2024-01-24 | GSE243441 | GEO
Project description:We demonstrate that Polo-like kinase 4(PLK4) is overexpressed in human bladder cancer (BC) cell lines and tissues, and its overexpression correlates with poor prognosis. PLK4 inhibition suppresses BC cell growth and induces G1 phase arrest via activating p38/p53/p21 pathway in vitro and in vivo. The data suggest that PLK4 might serve as a novel molecular target for BC treatment.
2021-07-29 | GSE180958 | GEO
Project description:Analysis of Copy Number for bladder cancer using Agilent Human Genome CGH Microarray Kit 4x44K
2024-01-12 | GSE164743 | GEO
Project description:Background: Current diagnosis and treatment of urinary bladder cancer (BC) has shown great progress with the utilization of microarrays. Purpose: Our goal was to identify common differentially expressed (DE) genes among clinically relevant subclasses of BC using microarrays. Methodology/Principal Findings: BC samples and controls, both experimental as well as publicly available datasets, were analyzed by whole genome microarrays. We grouped the samples according to their histology and defined the DE genes in each sample individually as well as in each tumor group, respectively. A dual analysis strategy was followed: First, experimental samples were analyzed and conclusions were extracted; and second, experimental sets were combined with publicly available microarray datasets and were further analyzed in search for common DE genes. The experimental dataset, identified 831 genes that were differentially expressed in all tumor samples, simultaneously. Moreover, 33 genes were up-regulated and 85 genes were down-regulated in all 10 BC samples compared to the 5 normal tissues, simultaneously. Hierarchical clustering partitioned tumor groups in accordance to their histology. K-means clustering of all genes and all samples, as well as clustering of tumor groups, presented 49 clusters. K-means clustering of common DE genes in all samples revealed 24 clusters. Genes manifested various differential patterns of expression, based on PCA. YY1 and NFκB were among the most common transcription factors that regulated the expression of the identified DE genes. Chromosome 1 contained 32 DE genes, followed by chromosomes 2 and 11, which contained 25 and 23 DE genes, respectively. Chromosome 21 had the least number of DE genes. GO analysis revealed the prevalence of transport and binding genes in the common down-regulated DE genes; the prevalence of RNA metabolism and processing genes in the up-regulated DE genes; as well as the prevalence of genes responsible for cell communication and signal transduction in the DE genes that were down-regulated in T1-Grade III tumors and up-regulated in T2/T3-Grade III tumors. Combination of all available samples revealed 17 common genes (BMP4, CRYGD, DBH, GJB1, KRT83, MPZ, NHLH1, TACR3, ACTC1, MFAP4, SPARCL1, TAGLN, TPM2, CDC20, LHCGR, TM9SF1 and HCCS) four of which participate in numerous pathways. Conclusions/Significance: The identification of the common DE genes among BC samples of different histology can provide further insight into the discovery of new putative markers. Oligos microarray chips (~57k genes) were obtained from GE HealthCare (IL) and AppliedMicroarrays (MA) (former Amersham Biosciences) (CodeLink 57k Human Whole Genome). Hybridization was performed with the CodeLink RNA amplification and Labeling kit as described by the manufacturer, utilizing the Cy5 fluorescent dye. Slides were scanned with a microarray scanner (ScanArray 4000XL). Images were generated with ScanArray microarray acquisition software (GSI Lumonics, USA). cRNAs from three experimental setups were used in single experiments with internal spikes as controls. The experimental setups consisted of 10 urinary BC samples of different histology and 5 control samples. The scanned images were further processed with the CodeLink Expression Analysis Software v5.0 from Amersham Biosciences (presently GE Health Care Inc.). The experimental setup was analyzed based on the reference-design as described previously. All tumor samples were compared against the mean value of the control samples. Raw microarray data are available as supplementary data and at the GEO microarray database. All microarray data are MIAME compliant. We used the following publicly available microarray datasets in our analysis: 1) GSE89 dataset (GDS183), comprised of 40 BC samples; 2) GSE3167 dataset (GDS1479), comprised of 60 samples (9 controls and 51 BC samples); 3) GSE7476 dataset, composed of 12 samples (3 controls and 9 BC samples) and 4) GSE12630 dataset, comprised of 19 BC samples. In total, our pooled microarray analysis was composed of 17 control samples (n=5, for the CodeLink platform; and n=12, for the rest microarray platforms) and 129 BC samples (n=10, for the CodeLink platform; and n=119, for the rest microarray platforms). Public data were used in their available normalized form, since background correction and normalization had already been performed.
2011-02-24 | E-GEOD-27448 | biostudies-arrayexpress
Project description:The purpose of this data set was to examine the effects of excess body condition (BC) loss in dairy cattle during lactation on oocyte and cumulus cell transcriptomes. Cells were collected from dairy cattle that lost BC (L group) or maintained/gained BC (M/G group) during the first 30 days in milk (DIM).
2022-07-20 | GSE182151 | GEO
Project description:Alterations in the epigenetic machinery in both tumor and immune cells contribute to bladder cancer (BC) development, constituting a promising target as an alternative therapeutic option. Here, we have explored the effects of a novel histone deacetylase (HDAC) inhibitor CM-1758, alone or in combination with immune checkpoint inhibitors (ICI) in BC. We determined the antitumor effects of CM-1758 in various BC cell lines together with the induction of broad transcriptional changes, with focus on the epigenetic regulation of PD-L1. Using an immunocompetent syngeneic mouse model of metastatic BC, we studied the effects of CM-1758 alone or in combination with anti-PD-L1 not only on tumor cells, but also in the tumor microenvironment. In vitro, we found that CM-1758 has cytotoxic and cytostatic effects either by inducing apoptosis or cell cycle arrest in BC cells at low micromolar levels. PD-L1 is epigenetically regulated by histone acetylation marks and is induced after treatment with CM-1758. We also observed that treatment with CM-1758 led to an important delay in tumor growth and a higher CD8+ T cell tumor infiltration. Moreover, anti-PD-L1 alone or in combination with CM-1758 reprogramed macrophage differentiation towards a M1-like polarization state and increased of pro-inflammatory cytokines systemically, yielding potential further cooperative antitumor effects. Our results suggest the possibility of combining HDAC inhibitors with immunotherapies for the management of advanced metastatic BC.
2024-01-04 | GSE245122 | GEO
Project description: Not available
| S-EPMC5647374 | biostudies-literature
Project description: Not available
| S-EPMC5583229 | biostudies-literature