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Elucidating the stromal expression pattern in response to tumor-derived Shh

ABSTRACT: Most tumors of the upper gastrointestinal tract are known to depend on an excessive expression of Shh. It was recently discovered that this Shh does not signal on the tumor cells, but rather the stromal cells that in turn produce an unknown set of reciprocal signals that act as growth- or survival cues for the tumor cells. This sequencing effort aims to identify the reciprocal signals. Mouse fibroblasts and Shh-expressing human pancreatic adenocarcinoma cells were either grown alone, or in a non-adherent coculture system. To be able to assess the effect of Shh on fibroblast gene expression (being the reciprocal signal), 5E1 blocking antibody was added to the cells and after 5 days, RNA was isolated. n=1

ORGANISM(S): Mus musculus

SUBMITTER: henk roelink

PROVIDER: E-GEOD-18245 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Elucidating the stromal expression pattern in response to tumor-derived Shh

Project description:Most tumors of the upper gastrointestinal tract are known to depend on an excessive expression of Shh. It was recently discovered that this Shh does not signal on the tumor cells, but rather the stromal cells that in turn produce an unknown set of reciprocal signals that act as growth- or survival cues for the tumor cells. This sequencing effort aims to identify the reciprocal signals.

2010-09-24 | GSE18245 | GEO

Expression data from adult Shh-responding astroglia cells in mice

Project description:Sonic hedgehog (Shh) signals via Gli transcription factors to promote maintenance and proliferation of neural stem cells in the adult mouse forebrain. We have analyzed the gene expression pattern in neurogenic Shh-responding astroglia (= neural stem cells ) in the subventicular zone of the lateral ventricle and dentate gyrus of the hippocampus in comparison to the non-neurogenic Shh-responding glia (=Bergman glia) in the cerebellum to identify the genes specifically involved in neurogenic function downstream of Shh signaling. In this dataset, we include the expression data obtained from FACS-sorted Gli1+ GFAP+ cells from microdissected SVZ, hippocampus and cerebellum. GFAP expression is based on hGFAP-GFP reporter line and Gli1 expression is lineage marked using Gli1-CreER;ROSA26-tdTomato mice. 15 Total samples were analyzed. We compared expression levels of SVZ vs. Cerebellum, Hippocampus vs. Cerebelllum to identify genes which had more than 4 fold change in expression levels with p < 0.01. From this narrowed list, we compared between SVZ and Hippocampus to identify the common genes up and down regulated. In addition, we also identified commonly expressed genes in hippocampus and SVZ at high level.

2013-09-18 | E-GEOD-50950 | biostudies-arrayexpress

Oncogene-dependent regulation of tumor cells via stromal reciprocal signalling

Project description:Cancer is a heterocellular disease composed of tumor cells and stromal cells. Although stromal cells are known to regulate cancer progression, oncogene-dependent signalling through heterocellular cancer systems remains poorly elucidated. Here, we describe KRASG12D-dependent ‘reciprocal’ signalling across tumor and stromal Pancreatic Ductal Adenocarcinoma (PDA) cells. Heterocellular multivariate phosphoproteomics demonstrates how an oncogenic cue (KRASG12D), a trans-cellular signal (SHH), and stromal cells drive a reciprocal response in tumor cells. KRASG12D-dependent reciprocal signalling regulates the tumor cell phosphoproteome, total proteome, and mitochondria activity via an IGFR1/AXL-AKT axis. The reciprocal KRASG12D signalling state requires a heterocellular context and is unreachable by cell-autonomous oncogenic KRAS alone. These findings provide evidence that oncogenic KRAS regulates tumor cells via heterocellular reciprocation. Comparison between FACS resolved iKRAS cells (previously in co-culture with PSCs) pertubed with a SHH antibody

2015-06-27 | E-GEOD-70351 | biostudies-arrayexpress

Posterior Second Heart Field (pSHF) transcriptomes of wild-type and Shh mutant mouse embryos

Project description:To understand Sonic hedgehog homolog (Shh)-mediated molecular networks in the posterior second heart field (pSHF), we have employed whole genome microarray expression profiling as a discovery platform to identify genes with Shh-dependent expressional changes. We microdissected the pSHF from E9.5 embryos and compared the Shh mutant samples with than of wild-type using Agilent 4x44k Mouse Whole Genome Arrays (n = 4 WT pools and 4 Shh - /- pools). Microdissected pSHF from E9.5 mouse embryos was molecularly verified by real-time PCR. Shh mutant embryos were compared with wild-type embryos. Four independnet pools of RNAs from each biological group were measured on 1-color Agilent Mouse Whole Genome Arrays (n = 3 WT pools and 4 Shh -/- pools).

2013-03-01 | E-GEOD-44754 | biostudies-arrayexpress

Transcription profiling of rat cerebellar granular cells cultured in the presence of Shh for 24h and then pulsed with Bmp2 or vehicle for up to 24h

Project description:Proliferating cerebellar granular cells were cultured in presence of Shh for 24h (3ug/ml) and then pulsed for additional 24h with Bmp2 or vehicle. Cells then were lysed and mRNA extracted. Microarray data from cells treated with Bmp2 was referred to the control not treated with Bmp2.

2007-06-07 | E-MEXP-1129 | biostudies-arrayexpress

Expression data from colon fibroblasts treated with Sonic hedgehog homolog (SHH)

Project description:Canonical Hedgehog (Hh) signaling regulates the expression of genes that are critical to the patterning and development of a variety of organ systems. In adult, both ligand-dependent and ligand-independent Hh pathway activation are known to promote tumorigenesis. Recent studies have shown that in tumors promoted by Hh ligand, activation occurs within the stromal microenvironment (Yauch et al., 2009). In situ hybridization of the pathway target gene, Ptch1, shows that signaling is located at stromal perivascular fibroblast-like cells in xenograft tumor sections derived from Hh-expressing colorectal cancer cell lines. To study the downstream genes regulated by Hh signaling, we treated a primary human colon myofibroblast, CCD-18Co, with SHH (1 ug/ml) or no treatment (control) in serum-free medium supplemented with 0.1% BSA for 72 hrs and performed microarray analysis (Affymetrix U133P) on these samples. Three biological replicates of SHH stimulated and three replicates of unstimulated primary colon myofibroblast cells CCD-18Co were used in the experiment to analyze their gene expression.

2011-05-17 | E-GEOD-29316 | biostudies-arrayexpress

Alterations in SHH signal transduction introduce a state of hypometabolism in sporadic Parkinson's disease

Project description:Sporadic Parkinson’s Disease (sPD) is a progressive neurodegenerative disorder caused by a combination of genetic and environmental factors, however, the etiology remains largely elusive. Here, we used human iPSCs from late onset sPD patients, which were cultivated in vitro for up to 60 passages and screened for known PD associated alterations. Following long-term in vitro cultivation, exclusively neural cells derived from sPD patients developed a reduced mitochondrial respiration and glucose consumption reflecting a sPD specific state of hypometabolism. Integrated analysis of transcriptome, proteome and non-targeted metabolome data identified the citric acid cycle as being the bottleneck in sPD metabolism. A 13C metabolic flux analysis further unraveled the α-ketoglutarate dehydrogenase complex as being central for a reduced flux through the citric acid cycle. This resulted in a substrate availability problem for the electron transport chain and thus a reduced mitochondrial ATP production. Notably, this alterations in basal cellular metabolism were introduced by altered SHH signal transduction due to dysfunctional primary cilia. Upon inhibiting the enhanced SHH signal transduction in sPD, glucose uptake and the activity of the α-ketoglutarate dehydrogenase complex could be restored. Thus, inhibiting overactive SHH signaling maybe a potential neuroprotective therapy for sPD.

2023-10-05 | PXD038399 | Pride

Transcription profiling by array of rat cerebellar granular neuronal precursor cells plated with Sonic Hedgehog (Shh) and then treated with the PKA activator DBA

Project description:Cerebellar granular neuronal precursors were plated in presence of Sonic Hedgehog (Shh) for 24h and then treated with the PKA activator Dibutyryl Cyclic Adenosine Monophosphate (DBA) for addittional 24h

2008-07-11 | E-MEXP-1668 | biostudies-arrayexpress

Expression data from adult Shh-responding astroglia cells in mice

2013-09-18 | GSE50950 | GEO

Cis-regulatory architecture of a brain-signaling center predates the origin of chordates

Project description:Genomic approaches have predicted hundreds of thousands of tissue specific cis-regulatory sequences, but the determinants critical to their function and evolutionary history are mostly unknown1-4. Here, we systematically decode a set of brain enhancers active in the zona limitans intrathalamica (zli), a signaling center essential for vertebrate forebrain development via the secreted morphogen, Sonic hedgehog (Shh)5,6. We apply a de novo motif analysis tool to identify six position-independent sequence motifs together with their cognate transcription factors that are essential for zli enhancer activity and Shh expression in the mouse embryo. Using knowledge of this regulatory lexicon, we discover novel Shh zli enhancers in mice, and a functionally equivalent element in hemichordates, indicating an ancient origin of the Shh zli regulatory network that predates the chordate phylum. These findings establish a paradigm for delineating functionally conserved enhancers in the absence of overt sequence homologies, and over extensive evolutionary distances. Gene expression profiles from the mouse zona limitans intrathalamica (ZLI) region at E10.5

2016-03-25 | E-GEOD-78005 | biostudies-arrayexpress

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