ABSTRACT: Identification of genes activated under CoCl2 treatment in an Sp1 dependent manner and under hypoxia without serum condition in an ovarian cancer cell line
Project description:To identify genes activated under CoCl2 treatment of a cancer cell line in an Sp1 dependent manner, we performed cDNA microarray analysis with an ovarian cancer cell line, in which Sp1 is silenced via RNA interference. Cells were transfected with scramble or Sp1 siRNA and cultured for 40 h. Cells were further cultured for 4 h under 0.5 mM CoCl2 exposure. Total RNA was isolated for cDNA microarray analysis.
Project description:To identify genes activated under CoCl2 treatment of a cancer cell line in an Sp1 dependent manner, we performed cDNA microarray analysis with an ovarian cancer cell line, in which Sp1 is silenced via RNA interference.
Project description:To identify genes activated under serum starvation and hypoxia condition in an SREBP1 dependent manner, we performed cDNA microarray analysis with an ovarian cancer cell line OVSAYO.
Project description:To identify genes activated under hypoxia (1%O2) and serum-free treatment of a cancer cell line, we performed cDNA microarray analysis with an ovarian cancer cell line, OVSAYO. Cells were cultured under normoxia /hypoxia (1%O2) and serum-plus/serum-minus conditions for 16 hours. Total RNA was isolated for cDNA microarray analysis.
Project description:To identify genes activated under hypoxia (1%O2) and serum-free treatment of a cancer cell line, we performed cDNA microarray analysis with an ovarian cancer cell line, OVSAYO.
Project description:HIF1α is a key regulator of hypoxia, however, the changes of its target genes in VSMCs under hypoxia were unknown. CoCl2 is a chemical hypoxia agent which leads to the stabilization of HIF1-α and the expression of hypoxia responsive genes, Therefore Hif1afl/fl and Hif1a△SMC VSMCs were treated with CoCl2 and performed microarray analysis. We used microarray to detail the gene expression of WT (Hif1afl/fl) mice and VSMC-specific HIF1α disruption (Hif1a△SMC) mice VSMCs treated with 150μM CoCl2 for 24hours.
Project description:Objective To explore the molecular mechanisms of retinopathy of prematurity (ROP) at whole genome scale using cultivated human fetal retinal microvascular endothelial cells (RMECs) under hypoxic condition. Study design Aborted fetuses with mean gestational age of 20-28 weeks at Guangdong Women and ChildrenM-bM-^@M-^Y Hospital were enrolled, 3 males and 2 females, with mean weight 610-2205 g. Primary RMECs were isolated by mechanical morcel and trypsin-collagenase digestion of eyeballs. Cultivated cells were treated with or without 150 M-NM-<M CoCl2 for 72 h. The dual-color microarray approach was adopted to compare gene expression profiling between treated RMECs and the paired untreated control using AgilentM-BM- SurePrint G3 Human GE 8x60K Microarray Kit. We applied average-linkage unsupervised hierarchical clustering and TreeView to visualize the results. The one class algorithm in the SAM software was used to screen the differentially expressed genes (DEGs) with a threshold set at fold-change >2.0 and q-value <0.05. Gene Ontology was employed for functional enrichment analysis. Results There were 326 DEGS between the hypoxia-induced group and untreated group. Of these genes, 198 were up-regulated in hypoxic RMECs, while other 128 hits were down-regulated. More importantly, altered expression genes in iron ion homeostasis pathway were highly enriched under hypoxic condition. Quantitative RT-PCR (qRT-PCR) was performed to validate the results obtained from microarray analysis. Conclusions Dysregulation of genes involved in iron homeostasis mediating oxidative damage may contribute to the ROP pathogenesis. Primary RMECs isolated from five subjects (3 males, 2 females) with mean weight 610-2205 g. CoCl2 induced hypoxia in primary RMECs vs. cultured cells without CoCl2 treatment. Biological replicates: five treated RMECs and paired untreated control. Dye-swap assays were performed for each sample.
Project description:Purpose: To study differential mRNA and precursor miRNA expression under hypoxia exposure in cancer cells. We treated ovarian cancer cell line A2780 under hypoxia condition at different time points. Normoxi acultured cells at corresponding time point were used as controls.
