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Whole Transcriptome Sequencing Identifies a Competitive Endogenous RNA Network that Regulates the Immunity of Bladder Cancer [miRNA-seq]

ABSTRACT: In this study, we performed whole-transcriptome sequencing of bladder tumors and their peritumoral tissues to identify differentially expressed circ-, lnc-, mi-, and mRNAs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE236933 | GEO | 2023/07/15

REPOSITORIES: GEO

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Whole Transcriptome Sequencing Identifies a Competitive Endogenous RNA Network that Regulates the Immunity of Bladder Cancer [RNA-seq]

Project description:In this study, we performed whole-transcriptome sequencing of bladder tumors and their peritumoral tissues to identify differentially expressed circ-, lnc-, mi-, and mRNAs.

2023-07-15 | GSE236932 | GEO

Whole Transcriptome Sequencing Identifies a Competitive Endogenous RNA Network that Regulates the Immunity of Bladder Cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-07-15 | GSE236935 | GEO

Comprehensive circular RNA expression profiling and competitive endogenous RNAs regulatory networks in distal cholangiocarcinoma

Project description:To explore the differentially expressed (DE) circular (circ)RNAs, competing endogenous RNAs networks, and potential biomarkers in distal cholangiocarcinoma (dCCA), using microarray analysis, a comprehensive circRNA expression profiling was constructed with six paired dCCA tumor and adjacent normal samples. A total of 171 DE circRNAs were identified. Three upregulated (hsa_circ_0060144, hsa_circ_0008274, and hsa_circ_0000673) and two downregulated circRNAs (hsa_circ_0139402 and hsa_circ_0001714) were validated with RT-qPCR in 40 dCCA patients. Among them, hsa_circ_0000673 had an idea prognostic efficiency (AUC=0.85, p<0.01) and high level of hsa_circ_0000673 was associated with late tumor stage (p<0.01), poor histodifferentiation (p=0.041), and residual tumor (p=0.044). Gene ontology analysis of the host genes of 171 DE circRNAs showed that “response to nutrient”, “adherens junction”, and “cell adhesion molecule binding” were mainly enriched in terms of biological process, cellular component, and molecular functions respectively. Nine target micro(mi)RNAs of the five DE circRNAs were screened out and enriched in cancer associated pathways. Thereafter, 188 DE mRNAs were predicted as target genes of the nine miRNAs. Finally, protein-protein interaction networks were constructed and 20 hubgenes were identified. This research provided a landscape of DE circRNAs in dCCA, constructed circRNA-miRNA-mRNA regulating networks, and identified hsa_circ_0000673 as a potential biomarker and target for treating dCCA.

2020-12-31 | GSE148561 | GEO

Identification of bladder cancer prognostic biomarkers using an ageing gene-related competitive endogenous RNA network.

Project description: Not available

| S-EPMC5762356 | biostudies-literature

Identification of competitive endogenous RNAs network in breast cancer.

Project description: Not available

| S-EPMC6536941 | biostudies-literature

c-Met activation leads to the establishment of a TGFβ receptor regulatory network required for bladder cancer invasion

Project description:Treatment of muscle-invasive bladder cancer remains a major clinical challenge. Aberrant HGF/c-MET upregulation and activation is frequently observed in bladder cancer correlating with cancer progression and invasion. However, the precise mechanisms underlying HGF/c-MET mediated invasion in bladder cancer remains unknown. As part of a negative feedback loop SMAD7 binds to the E3 ligase SMURF2 targeting the TGFβ receptor for degradation. Under these conditions SMAD7 acts as an agonist disrupting the intermolecular interactions within SMURF2, permitting SMURF2 activation. We demonstrate that HGF stimulates TGFβ signaling by inducing c-SRC mediated phosphorylation of SMURF2 at two tyrosine residues impeding SMAD7 binding and enhancing SMURF2 C2-HECT domain interaction, resulting in SMURF2 inhibition and TGFβ receptor stabilization. This upregulation of the TGFβ pathway by HGF leads to TGFβ-mediated EMT and invasion. Using biologically relevant orthotopic mouse models we show that inhibition of TGFβ signaling completely prevents HGF induced bladder cancer invasion. Furthermore, we make a rationale for the use of TGFβ receptor and MEK inhibitors in the treatment of high grade non-muscle-invasive bladder cancers or early stage muscle invasive bladder cancers.

2019-08-26 | PXD014736 | Pride

c-Met activation leads to the establishment of a TGFb regulatory network required for bladder cancer invasion

Project description:Aberrant c-Met activation and upregulation of its cognate ligand HGF are frequently observed in bladder cancer and have been shown to regulate downstream pathways involved in proliferation, motility, and invasion. The precise mechanism underlying HGF/c-MET mediated invasion in bladder cancer is partly addressed by this microarray dataset. HGF activates the canonical TGFb signaling pathway to enhance epithelial mesenchymal transition and bladder carcinoma invasion.

2019-08-23 | GSE104740 | GEO

Correlation of gene expression with bladder capacity in interstitial cystitis/bladder pain syndrome

Project description:Interstitial cystitis (IC) and bladder pain syndrome are terms used to describe a heterogenous chronic pelvic and bladder pain disorder of unknown etiology. The goal of this pilot study was to determine if gene expression profiling of bladder biopsy tissue from patients experiencing symptoms could be used to separate the patients based on some clinical parameter. Gene expression profiles in bladder biopsy tissue from patients with: (1) low bladder capacity (defined here as <400 ml upon hydordistension), (2) normal capacity (M-bM-^IM-%400 ml), and (3) controls were compared. Gene expression profiles from low bladder capacity tissues differed significantly from normal capacity and control tissue, suggesting gene expression profiling may be a useful tool for better understanding IC disease pathophysiology.

2014-05-13 | E-GEOD-57560 | biostudies-arrayexpress

Mouse Bladder LC-MS after bladder wall injection with Schistosoma haematobium eggs

Project description:Urogenital schistosomiasis (caused by Schistosoma haematobium) remains a major public health concern worldwide. In response to parasite egg deposition, the host bladder undergoes gross and molecular morphological changes relevant for disease manifestation. However, limited mechanistic studies to date imply that the molecular mechanisms underlying pathology have not been well-defined. We leveraged a mouse model of urogenital schistosomiasis to perform for the first time, proteome profiling of the early molecular events that occur in the bladder after exposure to S. haematobium eggs, and to elucidate the protein pathways involved in urogenital schistosomiasis-induced pathology. Purified S. haematobium eggs or control vehicle were microinjected into the bladder walls of mice. Mice were sacrificed seven days post-injection and bladder proteins isolated and processed for proteome profiling using mass spectrometry.

2022-01-23 | PXD029852 | Pride

Transcription profiling of rat bladder after inoculation with bladder cancer cells

Project description:Rat bladder cancer cells (AY-27 cell line) were inoculated intravesically into syngeneic female Fischer rats. The bladder was analyzed by histology and Affymetrix GeneChips and compared to bladders from sham operated and normal rats.

2009-04-22 | E-MTAB-104 | biostudies-arrayexpress

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