Systematic Analysis of Transcriptomic Profile of Renal Cell Carcinoma under Long-Term Hypoxia using Next-Generation Sequencing and Bioinformatics
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ABSTRACT:
PROVIDER: PRJNA421706 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6363050.fastq.gz | Fastqsanger.gz | |||
| SRR6363051.fastq.gz | Fastqsanger.gz | |||
| SRR6363052.fastq.gz | Fastqsanger.gz | |||
| SRR6363053.fastq.gz | Fastqsanger.gz | |||
| SRR6363054.fastq.gz | Fastqsanger.gz |
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Project description:Patients with clear cell renal cell carcinoma (ccRCC) are often diagnosed with both von Hippel-Lindau (VHL) mutations and the constitutive activation of hypoxia-inducible factor-dependent signaling. In this study, we investigated the effects of long-term hypoxia in 786-O, a VHL-defective renal cell carcinoma cell line, to identify potential genes and microRNAs associated with tumor malignancy. The transcriptomic profiles of 786-O under normoxia, short-term hypoxia, and long-term hypoxia were analyzed using next-generation sequencing. The results showed that long-term hypoxia promoted the ability of colony formation and transwell migration compared to normoxia. In addition, the differentially expressed genes induced by long-term hypoxia were involved in various biological processes including cell proliferation, the tumor necrosis factor signaling pathway, basal cell carcinoma, and cancer pathways. The upregulated (L1CAM and FBN1) and downregulated (AUTS2, MAPT, AGT, and USH1C) genes in 786-O under long-term hypoxia were also observed in clinical ccRCC samples along with malignant grade. The expressions of these genes were significantly correlated with survival outcomes in patients with renal cancer. We also found that long-term hypoxia in 786-O resulted in decreased expressions of hsa-miR-100 and has-miR-378, and this effect was also observed in samples of metastatic ccRCC compared to samples of non-metastatic ccRCC. These findings may provide a new direction for the study of potential molecular mechanisms associated with the progression of ccRCC.
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Project description:Hypoxia signature in Clear cell RCC A set of clear cell renal cell carcinomas were examined for the deregulation of hypoxia inducible and endocytosis regulated genes Tumor samples and Normal renal tissue GSE14762.rda contains an R data object
2009-02-09 | E-GEOD-14762 | biostudies-arrayexpress
Project description:Patients with clear cell renal cell carcinoma (ccRCC) are often diagnosed with both von Hippel-Lindau (VHL) mutations and the constitutive activation of hypoxia-inducible factor-dependent signaling. In this study, we investigated the effects of long-term hypoxia in 786-O, a VHL-defective renal cell carcinoma cell line, to identify potential genes and microRNAs associated with tumor malignancy. The transcriptomic profiles of 786-O under normoxia, short-term hypoxia and long-term hypoxia were analyzed using next-generation sequencing. The results showed that long-term hypoxia promoted the ability of colony formation and transwell migration compared to normoxia. In addition, the differentially expressed genes induced by long-term hypoxia were involved in various biological processes including cell proliferation, the tumor necrosis factor signaling pathway, basal cell carcinoma and cancer pathways. The upregulated (L1CAM and FBN1) and downregulated (AUTS2, MAPT, AGT and USH1C) genes in 786-O under long-term hypoxia were also observed in clinical ccRCC samples along with malignant grade. The expressions of these genes were significantly correlated with survival outcomes in patients with renal cancer. We also found that long-term hypoxia in 786-O resulted in decreased expressions of hsa-mir-100 and hsa-mir-378 and this effect was also observed in samples of metastatic ccRCC compared to samples of non-metastatic ccRCC. These findings may provide a new direction for the study of potential molecular mechanisms associated with the progression of ccRCC.
| S-EPMC5751259 | biostudies-literature
Project description:Hypoxia signature in Clear cell RCC A set of clear cell renal cell carcinomas were examined for the deregulation of hypoxia inducible and endocytosis regulated genes
2009-02-10 | GSE14762 | GEO
Project description:Background Extracellular vesicles (EVs) secreted by mesenchymal stromal cells (MSCs) provide significant protection against renal ischemia-reperfusion injury (IRI). Hypoxia is considered an important method for enhancing the tissue repair capabilities of MSCs. However, the specific effects of hypoxia on MSCs and MSC-EVs, as well as their therapeutic potential for renal IRI, remain unclear. In this study, we investigated the alterations in MSCs and the production of MSC-EVs following hypoxia pre-treatment, and further explored the key intrinsic mechanisms by which hypoxic MSC-EVs treat renal IRI. Methods Human umbilical cord MSCs were cultured under normoxic and hypoxic conditions. Proliferation and related pathways were measured, and RNA sequencing was used to detect changes in the transcription profile. MSC-EVs from both normoxic and hypoxic conditions were isolated and characterized. In vivo, the localization and therapeutic effects of MSC-EVs were assessed in a rat renal IRI model. Histological examinations were employed to assess the structure, proliferation, and apoptosis of IRI kidney tissue respectively. Renal function was measured by analyzing serum creatinine and blood urea nitrogen levels. In vitro, the therapeutic potential of MSC-EVs were measured in renal tubular epithelial cells injured by antimycin A. Protein sequencing analysis of hypoxic MSC-EVs was conducted, and the depletion of Glutathione S-Transferase Omega 1 (GSTO1) in hypoxic MSC-EVs was performed to verify its key role in alleviating renal injury. Results Hypoxia alters MSCs transcription, promotes their proliferation, and increases the production of EVs. Hypoxia-pretreated MSC-EVs exhibited a superior ability to mitigate renal IRI, enhancing proliferation and reducing apoptosis of renal tubular epithelial cells both in vivo and in vitro. Protein profiling of the EVs revealed an accumulation of numerous anti-oxidative stress proteins, with GSTO1 being particularly prominent. GSTO1 knock down was significantly reduced the antioxidant and therapeutic effects in renal IRI of hypoxic MSC-EVs. Conclusions Hypoxia significantly promotes MSC-EVs generation and enhances the therapeutic effect of EVs on renal IRI. The effect of antioxidant stress induced by GSTO1 is one of the most important underlying mechanisms. Our findings underscore that hypoxia-pretreated MSC-EVs represent a novel and promising therapeutic intervention for renal IRI.
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Project description:Although both of renal interstitial fibrosis (RIF) and renal carcinoma (RCC) are in hypoxic microenvironments, they underwent several contrary pathologicall changes. To investigate the potent targets in the RIF and RCC through transcriptome alterations of hypoxia compared with normoxia, we established hypoxia cell culture models, primarily simulating hypoxia microenvironments in RIF and RCC. By bioinformatics analysis, a certain number of significant differentially expressed genes (DEGs) among RIF and RCC were recognized. We then performed gene expression profiling analysis using data obtained from RNA-seqencing of 2 different cells cultured in hypoxia and normoxia.
2023-11-15 | GSE225253 | GEO
Project description:All mammalian cells need oxygen. Inadequate oxygen (hypoxia) triggers cellular responses for survival and the maintenance of homeostasis. A transcription factor, hypoxia-inducible factor (HIF), plays a central role in the hypoxia response; its activity is regulated by the oxygen-dependent degradation of the HIF-1a protein. Despite the ubiquity and importance of hypoxia responses, very little is known about the variation in the global transcriptional response to hypoxia among different cell types and its links to tissue and cell-specific diseases. We analyzed the temporal changes in global transcript levels in response to hypoxia in primary renal proximal tubule epithelial cells (RPTECs), breast epithelial cells, smooth muscle (SMs), and endothelial cells (ECs) with DNA microarrays. The extent of the transcriptional response to hypoxia was greatest in the renal tubule cells. This exaggerated response was associated with a uniquely high level of HIF-1a RNA in renal cells and could be diminished by reducing HIF-1a expression via RNA interference (RNAi). A gene-expression signature of the hypoxia response, derived from our studies of cultured mammary and renal tubular epithelial cells, showed coordinated variation in several human cancers, and was a strong predictor of clinical outcomes in both breast and ovarian cancers. In an analysis of a large, published gene-expression dataset from breast cancers, we found that the prognostic information in the hypoxia signature was virtually independent of that provided by the previously reported wound signature and more predictive of outcomes than any of the clinical parameters in current use. A stimulus or stress experiment design type is where that tests response of an organism(s) to stress/stimulus. e.g. osmotic stress, behavioral treatment Using regression correlation
2010-07-01 | E-GEOD-3537 | biostudies-arrayexpress
Project description:Renal interstitial fibrosis (RIF) is the prominent pathological characteristics of deteriorative chronic kidney disease (CKD), leading to peritubular capillary (PTC) rarefaction accompanied by significant hypoxia. However, the underlying mechanisms remain elusive. To deal with this, we constructed the chip sequencing of HK-2 cells in hypoxia to explore critical genes modulated by HIF-1α through peak annotation. Several biomarkers have been identified on the basis of bioinformatics and deserve further research.
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Project description:Glomerular diseases account for the majority of cases with chronic renal failure. Several genes have been identified with key relevance for glomerular function. Quite a few of these genes show a specific or preferential mRNA expression in the renal glomerulus. To identify additional candidate genes involved in glomerular function in humans we generated a human renal glomerulus-specific transcript dataset (GTD) by comparing gene expression profiles from human glomeruli and tubulointerstitium obtained from six transplant living donors using Affymetrix HG-U133A arrays. This analysis resulted in 677 genes with prominent overrepresentation in the glomerulus. Genes with ‘a prior’i established known prominent glomerular expression served for validation and were all found in the novel expression library (e.g. CDKN1, DAG1, DDN, EHD3, MYH9, NES, NPHS1, NPHS2, PDPN, PLA2R1, PLCE1, PODXL, PTPRO, SYNPO, TCF21, TJP1, WT1). The mRNA expression for several novel glomerulus-enriched genes identified in REGGEL was validated by qRT-PCR. Gene ontology and pathway analysis identified biological processes previously not reported to be of relevance in glomeruli including among others axon guidance. This finding was further validated by assessing the expression of the axon guidance molecules neuritin (NRN1) and roundabout receptor ROBO1 and -2. Glomerular disease associated differential mRNA regulation of ROBO2 was found in diabetic nephropathy. In summary, using a comparative strategy on microdissected nephrons novel transcripts with predominant expression in the human glomerulus could be identified. A systematic analysis of this glomerulus-specifc gene expression library allows the detection of target molecules and biological processes involved in glomerular biology and renal disease.
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