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Human PC-3 prostate cancer cells: Control (shNTC; non-target shRNA) vs. shETV4 knock down (shETV4)

ABSTRACT: Transcriptional profiling of human PC-3 prostate cancer cells lentivirally infected with non-target control (NTC) short hairpin (sh)RNA comparing with lentivirally shRNA mediated human ETV4 knock-down. Cells were either cultured for 24 hours at 20% oxygen tension or 0.2% oxygen. Goal was to determine (i) genes affected by hypoxia in PC-3 NTC cells and (ii) identification of hypoxically induced genes requiring ETV4 for hypoxic regulation. four condition experiment, shNTC at 20% and 0.2% oxygen and shETV4 at 20% and 0.2% oxygen for 24 hours. Biological replicates: 3 for each of the 4 conditions

ORGANISM(S): Homo sapiens

SUBMITTER: Daniel Stiehl

PROVIDER: E-GEOD-32385 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Synthetic transactivation screening reveals ETV4 as broad coactivator of hypoxia-inducible factor signaling.

Wollenick Kristin K Hu Jun J Kristiansen Glen G Schraml Peter P Rehrauer Hubert H Berchner-Pfannschmidt Utta U Fandrey Joachim J Wenger Roland H RH Stiehl Daniel P DP

Nucleic acids research 20111110 5

The human prolyl-4-hydroxylase domain (PHD) proteins 1-3 are known as cellular oxygen sensors, acting via the degradation of hypoxia-inducible factor (HIF) α-subunits. PHD2 and PHD3 genes are inducible by HIFs themselves, suggesting a negative feedback loop that involves PHD abundance. To identify novel regulators of the PHD2 gene, an expression array of 704 transcription factors was screened by a method that allows distinguishing between HIF-dependent and HIF-independent promoter regulation. Am ...[more]

PMID: 22075993

Similar Datasets

Human PC-3 prostate cancer cells: Control (shNTC; non-target shRNA) vs. shETV4 knock down (shETV4)

Project description:Transcriptional profiling of human PC-3 prostate cancer cells lentivirally infected with non-target control (NTC) short hairpin (sh)RNA comparing with lentivirally shRNA mediated human ETV4 knock-down. Cells were either cultured for 24 hours at 20% oxygen tension or 0.2% oxygen. Goal was to determine (i) genes affected by hypoxia in PC-3 NTC cells and (ii) identification of hypoxically induced genes requiring ETV4 for hypoxic regulation.

2011-12-06 | GSE32385 | GEO

Protein profiles following miRNA-23c and -4328 overexpression in prostate cancer cell lines, PC-3 and 22Rv1

Project description:The 22Rv1 and PC-3 cells were transduced with shMIMIC human lentiviral vectors (Horizon Discovery, Cambridge, UK) to stably overexpress miRNA-23c or -4328. The SMARTvector Non-Targeting Control (NTC) was expressed to serve as a negative control. The vectors contained a turbo green fluorescent protein (turboGFP) and a puromycin resistance gene cassette. After transduction, cells were cultured in a medium supplemented with 5 µg/mL puromycin (Takara Bio, Tokyo, Japan) for antibiotic selection. Overexpression was confirmed by monitoring the turboGFP by fluorescence microscopy and by RT-qPCR analysis of miRNA-23c and -4328 levels. Relative protein quantification was performed to compare protein expression in 22Rv1 and PC-3 single cell clones overexpressing miRNA-23c and -4328, compared to corresponding NTC cells. Single cell clones overexpressing either miRNA-23c (n = 3), -4328 (n = 3) or NTC (n = 3) were analyzed in triplicate.

2023-04-24 | PXD041683 | Pride

RNA-seq data set of EGFR mutant human non-small cell lung cancer cell lines PC9, HCC827, HCC4006 after NF2 knockout, YAP1 or WWTR1 overexpression or osimertinib treatment

Project description:Experiment was designed to study the effect of Hippo pathway on osimertinib resistance in non-small cell lung cancer cell lines. The specific comparisons investigated were: PC-9: NTC vs NF2 KO, EV vs YAP1 OE, EV vs WWTR1 OE, EV DMSO treated vs EV osimertinib treated HCC827: NTC vs NF2 KO, EV vs YAP1 OE, EV vs WWTR1 OE,EV DMSO treated vs EV osimertinib treated HCC4006: NTC vs NF2 KO, EV vs YAP1 OE, EV vs WWTR1 OE, EV DMSO treated vs EV osimertinib treated

2024-07-01 | E-MTAB-13831 | biostudies-arrayexpress

Gene expression changes upon knockdown or over-expression of the ETS gene ETV4 in prostate cancer cell lines

Project description:Chromosomal abnormalities that give rise to elevated expression levels of the ETS genes ETV1, ETV4, ETV5, or ERG are prevalent in prostate cancer, but the function of these transcription factors in carcinogenesis is not clear. Previous work implicates ERG, ETV1, and ETV5 as regulators of invasive growth but not transformation in cell lines. Here we show that the PC3 prostate cancer cell line provides a model system to study the over-expression of ETV4. Anchorage independent growth assays and microarray analysis indicate that high ETV4 expression is critical for the transformation phenotype of PC3 cells. However, genes up-regulated upon ETV4 over-expression were very similar to genes up-regulated by ETV1 over-expression in the RWPE-1 normal prostate cell line. Together these data indicate that the ETV4 dependent transformation phenotype observed in PC3 cells is due to the genetic background of the cell line, rather than a distinct characteristic of ETV4. Furthermore, these findings suggest that the function of ETS genes in prostate cancer may differ based on other genetic alterations in a tumor. Two sets of two color experiments. First is PC3 cells expressing one of two independent ETV4 shRNAs versus PC3 cells expressing a control shRNA (luciferase). Second is RWPE-1 cells expressing 3xFlag tagged ETV4 versus RWPE-1 cells with a control (empty) vector.

2011-03-24 | E-GEOD-21209 | biostudies-arrayexpress

Analysis of gene expression change by gefitinib treatment in gefitinib sensitive PC9 and resistant PC9.

Project description:We established a gefitinib-resistant cell line (PC-9GR), by serial exposure of gefitinib to PC-9, an originally gefitinib-sensitive lung cancer cell line (PC-9na), for long period.We collected total RNA from both PC-9 and PC-9GR and examined mRNA expression profile, comprehensively. Gefitinib induced gene expression was measured in human lung cancer cell line was measured at 48 hours after exposure to 1uM Gefitinib.

2012-06-30 | E-GEOD-38302 | biostudies-arrayexpress

Label-free proteomics analysis of the lysosome in HepG2 cells treated with different conditions

Project description:To identify which proteins are specifically regulated by CARNS2 via lysosomal degradation under hypoxia, we employed label-free quantitative proteomics analysis of isolated lysosome fractions of Nor-NTC, Hyp-NTC and Hyp-shCARNS2 HepG2 cells.

2023-11-22 | PXD047036 | Pride

Pancreatic Cancer HPAF/CD18 cells: Ecd knockdown vs Scrambled

Project description:Purpose: To study the expression and function of a novel cell cycle regulatory protein, human ecdysoneless (Ecd), during pancreatic cancer (PC) pathogenesis. Experimental Design: Immunohistochemical expression profiling of Ecd was done in non-neoplastic normal pancreatic tissues and pancreatic ductal adenocarcinoma lesions (from tissue microarray and Rapid Autopsy program) as well as precancerous PanIN lesions and metastatic organs. To analyze the biological significance of Ecd in PC progression, Ecd was stably knocked down in PC cell line followed by in vitro and in vivo functional assays. Results: Normal pancreatic ducts show very weak to no Ecd expression compared to significant positive expression in PC tissues (mean±SE composite score: 0.3±0.2 and 3.8±0.2 respectively, p<0.0001) as well as in PanIN precursor lesions with a progressive increase in Ecd expression with increasing dysplasia (PanIN-1 to PanIN-3). Analysis of matched primary tumors and metastases from PC patients revealed that Ecd is highly expressed in both primary pancreatic tumor and in distant metastatic sites. Further, knockdown of Ecd suppressed cell proliferation in vitro and tumorigenicity of PC cells in mice orthotopic tumors. Microarray study revealed that Ecd regulates expression of glucose transporter GLUT4 in PC cells and was subsequently shown to modulate glucose uptake, lactate production and ATP generation by PC cells. Finally, knockdown of Ecd also reduced level of pAkt, key signaling molecule known to regulate aerobic glycolysis in cancer cells. Conclusion: Ecd is a novel tumor promoting factor that is differentially expressed in pancreatic cancer and potentially regulates glucose metabolism within cancer cells.

2012-08-10 | GSE39988 | GEO

Transcription profiling of human dermal fibroblasts and lung microvascular endothelial cells irradiated with iron ions

Project description:Normal human dermal fibroblasts (NHDF) and human lung microvascular endothelial cells (HMVEC-L) were irradiated with iron ions (0, 0.2, 0.4 and 1 Gy, 1GEv/n) at Brookhaven National Labs (BNL). Aim of the study is to find differentially transcribed genes in dependance of radiation dose/source and cell type.

2009-04-25 | E-TABM-374 | biostudies-arrayexpress

RNA-seq of HeLa cells stably overexpressing SRSF6-GFP grown under normoxic and hypoxic conditions

Project description:We used HeLa cells that overexpress GFP-tagged SRSF6 (4-fold) were grown in normal conditions (Normoxia, 21% oxygen) or hypoxic conditions (Hypoxia, 0.2% oxygen). compared the binding pattern of SRSF6 between normoxia, 4h hypoxia and 24h hypoxia.

2023-01-03 | GSE198308 | GEO

Loss of colonic primary cilia promotes inflammation and carcinogenesis

Project description:Primary cilia (PC) are important signaling hubs in cells and we explored their role in colorectal cancer (CRC) and colitis. In the colon we found PC to be mostly present on different subtypes of fibroblasts and exposure of mice to either chemically induced colitis-associated colon carcinogenesis (CAC) or dextran sodium sulfate (DSS)-induced acute colitis decreased PC numbers. We employed conditional knock-out strains for the PC essential genes, Kif3A and Ift88, to generate mice with reduced numbers of PC on colonic fibroblasts. These mice showed an increased susceptibility in the CAC model as well as in DSS-induced colitis. Secretome and immunohistochemical analyses of DSS-treated mice displayed an elevated production of the pro-inflammatory cytokine IL-6 in PC-deficient colons. An inflammatory environment diminished PC presence in primary fibroblast cultures. This was triggered by IL-6 as identified by RNAseq analysis together with blocking experiments, suggesting an activation loop between IL-6 production and PC loss. Notably, an analysis of PC presence on biopsies of patients with ulcerative colitis as well as CRC patients revealed decreased numbers of PC on colonic fibroblasts in pathological versus surrounding normal tissue. Taken together, we provide evidence that a decrease in colonic PC numbers promotes colitis and CRC.

2022-11-29 | PXD033440 | Pride

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