Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA275502 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1804980.fastq.gz | Fastqsanger.gz | |||
| SRR1804981.fastq.gz | Fastqsanger.gz | |||
| SRR1804982.fastq.gz | Fastqsanger.gz | |||
| SRR1804979.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: The oxidation resistance gene 1 (OXR1) is crucial for protecting against oxidative stress, limiting neurodegeneration and maintaining normal lifespan in eukaryotes. However, the molecular function of OXR1 is still unknown. Previously we showed that human OXR1 regulates expression of antioxidant genes GPX2 and HO-1 via the p21 signaling pathway. To examine the role of hOXR1 in global transcription regulation during cellular stress, we employed RNA sequencing to investigate the transcription profile in hOXR1 depleted HeLa cells. Methods: Control siRNA (siCon) and human OXR1 siRNA (siOXR1) transfected HeLa cells were either harvested directly (siCon_NT, siOXR1_NT) or exposed to 0.5 mM H2O2 for 1 h and then harvested immediately without recovery (siCon_R0h, siOXR1_R0h). Total RNA pooled from duplicate samples was used for RNA sequencing on an Illumina HiSeq2000 platform. The sequence reads that passed quality filters were analyzed at gene level. The Blast2GO program was used to generate gene ontology (GO) annotation of differentially expressed genes (DEGs).The WEGO software was used to further perform GO functional classification and to predict pathways affected. qRTM-bM-^@M-^SPCR validation was performed using SYBR Green assays. Results: In total, in non-treated and hydrogen peroxide exposed cells, hOXR1 depletion results in the down-regulation of 554 genes and the up-regulation of 253 genes. These differentially expressed genes include transcription factors (i.e. HIF1A, SP6, E2F8 and TCF3) and numerous genes of the p53 signaling pathway involved in cell-cycle arrest (i.e. cyclin D, CDK6 and p21) and apoptosis (i.e. CytC and CASP9). Western blot analysis reveals that hOXR1 suppresses CASP9 protein expression and reduces post-translational cleavage into its active form. After exposure to hydrogen peroxide (1 h), 56 early response genes were up-regulated in hOXR1 depleted cells, in which 38 of these genes were not induced in control cells. In addition, a subset of the commonly up-regulated early response genes showed a stronger induction in hOXR1 depleted cells (i.e. FOS, JUN and DUSP1). Out of a total of 52 differentially expressed transcription factors in hOXR1 depleted cells under normal physiology and oxidative stress condition, 14 genes (including HIF1A, STAT5A, E2F8 and TCF3) are differentially regulated under H2O2 treatment in hOXR1 silenced cells as compared to control cells. Finally, we demonstrate that hOXR1 depleted cells undergo cell cycle arrest in G2/M phase during oxidative stress. Conclusions: Human OXR1 is important for regulation of the early stress response to oxidative stress in HeLa cells. HOXR1 modulates the p53 signaling pathway via regulation of genes involved in cell cycle arrest, apoptosis and anti-oxidation. Further, hOXR1 regulates numerous transcription factors of importance for cellular stress responses. In summary, hOXR1 may act as a sensor of cellular oxidative stress to regulate the transcriptional networks required to detoxify reactive oxygen species (ROS) and modulate cell cycle arrest and cell death (apoptosis). The mRNA profiles of hOXR1 depleted and control Hela cells with or without H2O2 treatment 1 h were generated by RNA sequencing using Illumina Hiseq 2000.
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Project description:The goal of this experiment was to determine the role of the lncRNA DINO in the DNA damage response in regulating transcription factor occupancy of human fibroblasts. DINO, an inducible long noncoding in respose to DNA damage, is required for cell cycle arrest and induction of several p53 regulated genes. We hypothesized that ATACseq in DINO-depleted cells may uncover a role for DINO in transcription factor recruitment to p53 responsive genes following DNA damage.
2016-09-26 | GSE76417 | GEO
Project description:Transcriptome analysis of control and MALAT1 lncRNA-depleted RNA samples from human diploid lung fibroblasts [WI38] The long noncoding MALAT1 RNA is upregulated in cancer tissues and its elevated expression is associated with hyper-proliferation, but the underlying mechanism is poorly understood. We demonstrate that MALAT1 levels are regulated during normal cell cycle progression. Genome-wide transcriptome analyses in normal human diploid fibroblasts reveal that MALAT1 modulates the expression of cell cycle genes, and is required for G1/S and mitotic progression. Depletion of MALAT1 leads to activation of p53 and its target genes. The cell cycle defects observed in MALAT1-depleted cells are sensitive to p53 levels, indicating that p53 is a major downstream mediator of MALAT1 activity. Furthermore, MALAT1-depleted cells display reduced expression of B-MYB (Mybl2), an oncogenic transcription factor involved in G2/M progression, due to altered binding of splicing factors on B-MYB pre-mRNA and aberrant alternative splicing. In human cells, MALAT1 promotes cellular proliferation by modulating the expression and/or pre-mRNA processing of cell cycle-regulated transcription factors. These findings provide mechanistic insights on the role of MALAT1 in regulating cellular proliferation.
2013-01-29 | GSE43830 | GEO
Project description:To test the hypothesis that circRNAs might encode functional peptides in mammalian cells, we studied the long intergenic non-protein coding RNA, p53 induced transcript (LINC-PINT), which was previously reported as a tumor suppressor and connected p53 activation with polycomb repressive complex 2 (PRC2). We selected this long noncoding RNA (lncRNA) for further analysis because LINC-PINT has a long exon 2 which in accordance with the bioinformatical analyzed circular RNA standard.The following immunoblotting showed 87aa peptide level also decreased, indicating that this peptide is encoded by circPINTexon2. We name this circRNA encoded peptide PINT87aa. To investigate the possible regulatory role of PINT87aa, we did the expression micro array in PINT87aa stably transfect U251 or U87 glioblastoma cells and their control cells. The array analysis reveals that PINT87aa may involve in the cell cycle regulation, anti-apoptosis effects and multiple oncogenic signaling pathway activation.
2015-11-04 | E-GEOD-74610 | biostudies-arrayexpress
Project description:It has been recently shown that the transcription factor p53 induces the expression of multiple lincRNAs. However, relatively little is known about the role that lincRNAs play in this pathway. Here we characterize a lincRNA named PINT (p53 Induced Noncoding Transcript). We show that PINT is a ubiquitously expressed lincRNA that is finely regulated by p53. In mouse cells, PINT promotes cell proliferation and survival by regulating the expression of genes of TGF-beta, MAPK and p53 pathways. PINT is a nuclear lincRNA that directly interacts with Polycomb Repressive Complex 2 (PRC2), being required for PRC2 targeting of specific genes for repression. Furthermore, PINT functional activity is dependent on PRC2 expression, representing a connection between the p53 pathway and epigenetic regulation by PRC2. We have also identified PINT human ortholog (hPINT), which presents suggestive analogies with the mouse lincRNA. hPINT is similarly regulated by p53, and its expression correlates significantly with the same cellular pathways as the mouse ortholog, including the p53 pathway. Interestingly, hPINT is significantly downregulated in colon cancer, representing a novel tumor suppressor candidate. Our results not only help our understanding of the role of p53 and lincRNAs in cancer, but also contribute to the open debate regarding the utility of mouse models for the study of lincRNAs. Normal tissue located at least 20 cm away from a tumor was obtained through surgical resection from patients of colorectal cancer. Total RNA was extracted and subjected to microarray analysis.
2013-08-09 | E-GEOD-46271 | biostudies-arrayexpress
Project description:Purpose: The oxidation resistance gene 1 (OXR1) is crucial for protecting against oxidative stress, limiting neurodegeneration and maintaining normal lifespan in eukaryotes. However, the molecular function of OXR1 is still unknown. Previously we showed that human OXR1 regulates expression of antioxidant genes GPX2 and HO-1 via the p21 signaling pathway. To examine the role of hOXR1 in global transcription regulation during cellular stress, we employed RNA sequencing to investigate the transcription profile in hOXR1 depleted HeLa cells. Methods: Control siRNA (siCon) and human OXR1 siRNA (siOXR1) transfected HeLa cells were either harvested directly (siCon_NT, siOXR1_NT) or exposed to 0.5 mM H2O2 for 1 h and then harvested immediately without recovery (siCon_R0h, siOXR1_R0h). Total RNA pooled from duplicate samples was used for RNA sequencing on an Illumina HiSeq2000 platform. The sequence reads that passed quality filters were analyzed at gene level. The Blast2GO program was used to generate gene ontology (GO) annotation of differentially expressed genes (DEGs).The WEGO software was used to further perform GO functional classification and to predict pathways affected. qRT–PCR validation was performed using SYBR Green assays. Results: In total, in non-treated and hydrogen peroxide exposed cells, hOXR1 depletion results in the down-regulation of 554 genes and the up-regulation of 253 genes. These differentially expressed genes include transcription factors (i.e. HIF1A, SP6, E2F8 and TCF3) and numerous genes of the p53 signaling pathway involved in cell-cycle arrest (i.e. cyclin D, CDK6 and p21) and apoptosis (i.e. CytC and CASP9). Western blot analysis reveals that hOXR1 suppresses CASP9 protein expression and reduces post-translational cleavage into its active form. After exposure to hydrogen peroxide (1 h), 56 early response genes were up-regulated in hOXR1 depleted cells, in which 38 of these genes were not induced in control cells. In addition, a subset of the commonly up-regulated early response genes showed a stronger induction in hOXR1 depleted cells (i.e. FOS, JUN and DUSP1). Out of a total of 52 differentially expressed transcription factors in hOXR1 depleted cells under normal physiology and oxidative stress condition, 14 genes (including HIF1A, STAT5A, E2F8 and TCF3) are differentially regulated under H2O2 treatment in hOXR1 silenced cells as compared to control cells. Finally, we demonstrate that hOXR1 depleted cells undergo cell cycle arrest in G2/M phase during oxidative stress. Conclusions: Human OXR1 is important for regulation of the early stress response to oxidative stress in HeLa cells. HOXR1 modulates the p53 signaling pathway via regulation of genes involved in cell cycle arrest, apoptosis and anti-oxidation. Further, hOXR1 regulates numerous transcription factors of importance for cellular stress responses. In summary, hOXR1 may act as a sensor of cellular oxidative stress to regulate the transcriptional networks required to detoxify reactive oxygen species (ROS) and modulate cell cycle arrest and cell death (apoptosis).
2015-02-16 | GSE65949 | GEO
Project description:It has been recently shown that the transcription factor p53 induces the expression of multiple lincRNAs. However, relatively little is known about the role that lincRNAs play in this pathway. Here we characterize a lincRNA named PINT (p53 Induced Noncoding Transcript). We show that PINT is a ubiquitously expressed lincRNA that is finely regulated by p53. In mouse cells, PINT promotes cell proliferation and survival by regulating the expression of genes of TGF-beta, MAPK and p53 pathways. PINT is a nuclear lincRNA that directly interacts with Polycomb Repressive Complex 2 (PRC2), being required for PRC2 targeting of specific genes for repression. Furthermore, PINT functional activity is dependent on PRC2 expression, representing a connection between the p53 pathway and epigenetic regulation by PRC2. We have also identified PINT human ortholog (hPINT), which presents suggestive analogies with the mouse lincRNA. hPINT is similarly regulated by p53, and its expression correlates significantly with the same cellular pathways as the mouse ortholog, including the p53 pathway. Interestingly, hPINT is significantly downregulated in colon cancer, representing a novel tumor suppressor candidate. Our results not only help our understanding of the role of p53 and lincRNAs in cancer, but also contribute to the open debate regarding the utility of mouse models for the study of lincRNAs. Inhibition of PINT or p53 gene expression and subsequent treatment with 150 nM doxorubicine for 12h in MEF LSL p53 +/+ cells.
2013-08-09 | E-GEOD-46247 | biostudies-arrayexpress
Project description:In an effort to identify genes whose expression is regulated by activated PI3K signaling, we performed microarray analysis and subsequent qRT-PCR on an isogenic set of PTEN gene-targeted human cancer cells. Numerous p53 effectors were upregulated following PTEN deletion, including p21, GDF15, PIG3, NOXA, and PLK2. Stable depletion of p53 led to reversion of the gene expression program. Western blots revealed that p53 was stabilized in HCT116 PTEN-/- cells via an Akt1-dependent and p14ARF-independent mechanism. Stable depletion of PTEN in untransformed human fibroblasts and epithelial cells also led to upregulation of p53 and senescent-like growth arrest. Simultaneous depletion of p53 rescued this phenotype, enabling PTEN-depleted cells to continue proliferating. Next, we tested whether oncogenic PIK3CA, like inactivated PTEN, could activate p53. Retroviral expression of oncogenic human PIK3CA in MCF10A cells led to activation of p53 and upregulation of p53-regulated genes. Stable depletion of p53 reversed these PIK3CA-induced expression changes and synergized with oncogenic PIK3CA in inducing anchorage-independent growth. Finally, targeted deletion of an endogenous allele of oncogenic but not wild-type PIK3CA in a human cancer cell line led to a reduction in p53 levels and a decrease in the expression of p53-regulated genes. These studies demonstrate that activation of PI3K signaling by mutations in PTEN or PIK3CA can lead to activation of p53-mediated growth suppression in human cells, indicating that p53 can function as a brake on PIP3-induced mitogenesis during human cancer pathogenesis. Experiment Overall Design: Two HCT116 PTEN+/+ cell lines (parental cells and a clone with random integration of the targeting vector) and three independently-derived HCT116 PTEN-/- cell lines were studied
2008-06-14 | E-GEOD-6263 | biostudies-arrayexpress