YBX1-dependent hypoxia-induced modulation of gene expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Hani Goodarzi
PROVIDER: E-GEOD-63562 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:In order to identify YBX1-dependent targets that are modulated upon changing the levels of endogenous tRFs, we used transient transfection of antisense locked-nucleic acids (LNAs) against tRFAsp, tRFGly, tRFGlu, and tRFTyr followed by alpha-amanitine treatment, RNA extraction at time points 0 and 8hr post-treatment, and transcriptomic profiling. Synthetic antisense locked-nucleic acids (LNAs) targeting the YBX1 binding site on tRFAsp, tRFGly, tRFGlu, and tRFTyr were transfected into control and YBX1-knockdown cells to identify YBX1-dependent targets whose stabilities are modulated due to tRF loss-of-function. We used alpha-amanitine mediated inhibition of RNA-polymerase to measure transcript stability across the entire transcriptome.
2015-05-08 | E-GEOD-63565 | biostudies-arrayexpress
Project description:In order to test whether inhibition of tRFs induced under hypoxia would counteract the YBX1-dependent reduction of target transcripts, we used transient transfection of antisense locked-nucleic acids (pooled LNAs) against tRFAsp, tRFGly, tRFGlu, and tRFTyr under hypoxia followed by microarray profiling. Synthetic antisense locked-nucleic acids (LNAs) targeting the YBX1 binding site on tRFAsp, tRFGly, tRFGlu, and tRFTyr were transfected (as a pool) in control and YBX1-knockdown cells under hypoxia to assess the consequences of inhibiting tRFs induced in hypoxic MDA-parental cells.
2015-05-08 | E-GEOD-63563 | biostudies-arrayexpress
Project description:In order to identify YBX1-dependent targets that are modulated under hypoxic conditions, we used control and YBX1 knockdown cells grown under normoxia and hypoxia to profile gene expression levels.
2015-05-08 | GSE63562 | GEO
Project description:In order to identify YBX1-dependent targets that are modulated upon changing the levels of endogenous tRFs, we used transient transfection of antisense locked-nucleic acids (LNAs) against tRFAsp, tRFGly, tRFGlu, and tRFTyr followed by microarray profiling. Synthetic antisense locked-nucleic acids (LNAs) targeting the YBX1 binding site on tRFAsp, tRFGly, tRFGlu, and tRFTyr were transfected into control and YBX1-knockdown cells to identify YBX1-dependent targets that are modulated due to tRF loss-of-function.
2015-05-08 | E-GEOD-63564 | biostudies-arrayexpress
Project description:In order to test whether inhibition of tRFs induced under hypoxia would counteract the YBX1-dependent reduction of target transcripts, we used transient transfection of antisense locked-nucleic acids (pooled LNAs) against tRFAsp, tRFGly, tRFGlu, and tRFTyr under hypoxia followed by microarray profiling.
2015-05-08 | GSE63563 | GEO
Project description:Glycolysis is upregulated in cells under specific conditions, such as hypoxia and high energy demand, to achieve the metabolic requirements for continued cell proliferation. However, the mechanism of this increased glycolytic rate remains poorly understood. In the budding yeast Saccharomyces cerevisiae, we discovered that hypoxia induces concentration of many glycolytic enzymes, including the Pfk2p subunit of the ratelimiting enzyme, phosphofructokinase, into a single, non-membrane-bound granule that we define as the "glycolytic body" or "G body". Pfk2p localization to G bodies depends on its N-terminal, intrinsically disordered region. In order to identify factors important for G body formation, we conducted a yeast kinome screen and identified the AMP kinase ortholog, Snf1p, to be required for the localization of multiple glycolytic enzymes to G bodies. Further, proteomic analyses of purified G bodies identified a core set of resident factors, many of which are essential for G body integrity. Cells incapable of forming G bodies in hypoxic conditions display abnormal cell division and produce inviable daughter cells. Conversely, cells that form G bodies show increased glucose consumption and decreased levels of glycolytic intermediates. Importantly, G bodies also form in human, hepatocarcinoma cells upon hypoxic stress. Together, our results suggest that G body formation is a conserved, adaptive response to increase glycolytic output during hypoxia or tumorigenesis.
2017-07-24 | PXD006686 | Pride
Project description:In order to identify YBX1 binding sites on endogenous RNA, we performed HITS-CLIP on endogenous YBX1 We used a previously published method to perform HITS-CLIP on endogenous YBX1 (Licatalosi D, et al. 2008, Nature 456:464-U22)
2015-05-08 | E-GEOD-63604 | biostudies-arrayexpress
Project description:In order to identify YBX1 binding sites on tRNA fragments, we performed small-RNA HITS-CLIP on endogenous YBX1 We used a previously published method to perform HITS-CLIP on endogenous YBX1 (Chi SW, et al. 2009, Nature 460:479)
2015-05-08 | E-GEOD-63597 | biostudies-arrayexpress
Project description:YBX1 is a multifunctional protein involved in the control of transcription and translation. We identified YBX1 as an target of MEK/ERK signaling in colorectal cancer cell lines. We performed a ChIP-chip analysis of HCT116 cells to identify new potential target genes of YBX1. Comparison of input DNA fragments with fragments coprecipitated with YBX1 in HCT116 cells.
2010-10-09 | E-GEOD-18337 | biostudies-arrayexpress
Project description:Hypoxia is one of the major driving forces mediating tumor angiogenesis, aggressiveness, as well as resistance to chemo- and radiotherapy. It has also been suggested to play important roles in stem cell maintenance for both normal and cancer tissues. However, the mechanisms by which hypoxia-driven epigenetic changes modulate tumorigenesis remain poorly understood. As the histone H3 lysine 9 (H3K9) demethylase Jmjd1a and methyltransferase G9a are upregulated downstream targets of hypoxia, we focused on these two catalytically opposing epigenetic modifiers to address this question. Through the use of homozygous Jmjd1a and G9a knockout mouse embryonic stem (ES) cells, we found that Jmjd1a was not required for stem cell self-renewal and that anti-angiogenesis related genes were epigenetically dysregulated in both Jmjd1a- and G9a deficient ES cells under hypoxic conditions, accompanied by corresponding changes in H3K9 dimethylation and H3K4 trimethylation levels in the proximal promoter regions of these target genes. Most importantly, these genetic alterations led to opposing tumor phenotypes: loss of Jmjd1a results in increased tumor growth, whereas loss of G9a produces smaller tumors. These findings provide new insights on the importance of hypoxia signalling in regulating the epigenetic status and expression of angiogenesis genes that promote tumor progression. 63 microarray samples consisting of 7 mouse ES cell lines of which 2 are wild type (control), 2 Jmjd1a knockout, 2 G9a knockout and 1 G9a knockout that was reconstituted for G9a (G9a control). Each cell line and condition was seeded at 3 different densities (2X10^5, 4X10^5 and 6X10^5) in 6 cm dishes to control for the effects of cell confluency on gene expression. 18 hours after plating, the cells were subjected to normoxia (21% O2) for 24 hours (control), normoxia 20 hours followed by hypoxia (1% O2) for 4 hours (acute hypoxia) and 24 hours hypoxia (chronic treatment). Total RNA was harvested from all samples for microarrays after the 24 hour treatments.
2014-07-30 | E-GEOD-35061 | biostudies-arrayexpress