Gene expression analyses of CWR22Res Nsi (non-silencing) control and with stable knockdown of Sprouty2 (SPRY2)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE108456 | GEO | 2018/03/13
REPOSITORIES: GEO
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Project description:Gene expression analyses of CWR22Res Nsi (non-silencing) control and with stable knockdown of Sprouty2 (SPRY2)
| PRJNA427327 | ENA
Project description:The role of SPROUTY2 (SPRY2) in human colon cancer is controversial. Our data support a tumorigenic action of SPRY2. We use microarrays to identify SPRY2 target genes in human SW480 ADH colon carcinoma cell line.
2016-08-01 | GSE56941 | GEO
Project description:The role of SPROUTY2 (SPRY2) in human colon cancer is controversial. Our data support a tumorigenic action of SPRY2. We use microarrays to identify SPRY2 target genes in human SW480 ADH colon carcinoma cell line. RNA was obtained from SW480 ADH cells, Mock transfected or transfected with WT or two differents SPRY2 genes mutants. Hybridization was performed on Affymetrix microarrays. We performed three independent experiments. Each experiment was conducted in triplicate.
2016-08-01 | E-GEOD-56941 | biostudies-arrayexpress
Project description:Sprouty2 (Spry2) and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) are both well-established regulators of receptor tyrosine kinase (RTK) signaling, and knockdown of Spry2 or PTEN enhances axon regeneration of dorsal root ganglia (DRG) neurons. The major role of Spry2 is the inhibition of the rat sarcoma RAS/extracellular signal-regulated kinase (ERK) pathway, whereas PTEN acts mainly as an inhibitor of the phosphoinositide 3-kinase (PI3K)/Akt pathway. In non-neuronal cells, Spry2 increases the expression and activity of PTEN, and PTEN enhances the amount of Spry2 by the inhibition of the microRNA-21 (miR-21) that downregulates Spry2. Applying dissociated DRG neuron cultures from wild-type (WT) or Spry2 deficient mice, we demonstrate that PTEN protein was reduced after 72 h during rapid axonal outgrowth on the laminin substrate. Furthermore, PTEN protein was decreased in DRG cultures obtained from homozygous Spry2-/- knockout mice. Vice versa, Spry2 protein was reduced by PTEN siRNA in WT and heterozygous Spry2+/- neurons. Knockdown of PTEN in DRG cultures obtained from homozygous Spry2-/- knockout mice promoted axon elongation without increasing axonal branching. Activation of Akt, but not ERK, was stronger in response to PTEN knockdown in homozygous Spry2-/- DRG neurons than in WT neurons. Together, our study confirms the important role of the signaling modulators Spry2 and PTEN in axon growth of adult DRG neurons. Both function as endogenous inhibitors of neuronal growth factor signaling and their simultaneous knockdown promotes axon elongation more efficiently than the single knockdown of each inhibitor. Furthermore, Spry2 and PTEN are reciprocally downregulated in adult DRG neuron cultures. Axon growth is influenced by multiple factors and our results demonstrate that the endogenous inhibitors of axon growth, Spry2 and PTEN, are co-regulated in adult DRG neuron cultures. Together, our data demonstrate that combined approaches may be more useful to improve nerve regeneration than targeting one single inhibitor of axon growth.
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Project description:We recently showed that inactivation of the WASF3/WAVE3 gene in breast cancer cells results in loss of cell motility and invasion in vitro and metastasis in vivo. To obtain a better understanding of molecular mechanisms of action of WASF3, we have established the stable WASF3 knockdown MDA-MB-231 cells using shRNA strategy. We used microarrays to detail the global programme of gene expression after silencing WASF3 and identified distinct classes of up or down-regulated genes associated with breast cancer cell migration and motility The three stable WASF3 knockdown single clones and three control clones were selected for RNA extraction and hybridization on Affymetrix microarrays. To identify altered gene expression patterns in the knockdown cells, we compared gene expression levels between three different knockdown and three different control clones.
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Project description:The rat has served as an excellent model for studies on animal physiology and as a model for human diseases such as diabetes and alcoholism; however, genetic studies have been limited because of the inability to knock out genes. Our goal was to produce heritable deficiencies in specific gene function in the rat using RNA interference to knock down gene expression in vivo. Lentiviral-mediated transgenesis was used to produce rats expressing a short hairpin RNA targeting Dazl, a gene expressed in germ cells and required for fertility in mice. Germ-line transmission of the transgene occurred, and its expression correlated with significant reductions in DAZL protein levels and male sterility, and the knockdown was stable over multiple generations (F(1)-F(3)). This study demonstrates an efficient system by which directed reverse genetic analysis can now be performed in the rat.
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Project description:When a duplicate gene has no apparent loss-of-function phenotype, it is commonly considered that the phenotype has been masked as a result of functional redundancy with the remaining paralog. This is supported by indirect evidence showing that multi-copy genes show loss-of-function phenotypes less often than single-copy genes and by direct tests of phenotype masking using select gene sets. Here we take a systematic genome-wide RNA interference approach to assess phenotype masking in paralog pairs in the Caenorhabditis elegans genome. Remarkably, in contrast to expectations, we find that phenotype masking makes only a minor contribution to the low knockdown phenotype rate for duplicate genes. Instead, we find that non-essential genes are highly over-represented among duplicates, leading to a low observed loss-of-function phenotype rate. We further find that duplicate pairs derived from essential and non-essential genes have contrasting evolutionary dynamics: whereas non-essential genes are both more often successfully duplicated (fixed) and lost, essential genes are less often duplicated but upon successful duplication are maintained over longer periods. We expect the fundamental evolutionary duplication dynamics presented here to be broadly applicable.
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Project description:The molecular drivers for the AR signaling reprogramming in castration-resistant prostate cancer remain to be determined. In this study, we hypothesize that increased AR expression in conjunction with lower-level androgens, which is a typical condition in prostate cancer cells receiving androgen deprivation therapy, is a major driving force of the reprogramming. To test this, we used LNCaP model with inducible overexpression of AR to examine the acute effects of AR overexpression stimulated by low-dose DHT (0.1nM) on AR cistrome.
2022-11-21 | GSE211639 | GEO
Project description:Purpose: The goal of this study is to identify p300-regulated genes.
2022-05-13 | GSE131231 | GEO
Project description:The importance of transgenerationally inherited epigenetic states to organismal fitness remains unknown as well-documented examples are often not amenable to mechanistic analysis or rely on artificial reporter loci. Here we describe an induced silenced state at an endogenous locus that persists, at 100% transmission without selection, for up to 13 generations. This unusually persistent silencing enables a detailed molecular genetic analysis of an inherited epigenetic state. We find that silencing is dependent on germline nuclear RNAi factors and post-transcriptional mechanisms. Consistent with these later observations, inheritance does not require the silenced locus, and we provide genetic evidence that small RNAs embody the inherited silencing signal. Notably, heritable germline silencing directs somatic epigenetic silencing. Somatic silencing does not require somatic nuclear RNAi but instead requires both maternal germline nuclear RNAi and chromatin-modifying activity. Coupling inherited germline silencing to somatic silencing may enable selection for physiologically important traits.
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