Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Indraccolo_Notch3

ABSTRACT: Notch3 expression was analyzed in 20 patients suffering from colorectal carcinoma (CRC) and their corresponding colonic normal (NC) tissue.

ORGANISM(S): Homo sapiens

DISEASE(S): colorectal carcinoma

SUBMITTER: Elisabeth Naschberger

PROVIDER: E-MEXP-3188 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Notch3 signalling promotes tumour growth in colorectal cancer.

Serafin Valentina V Persano Luca L Moserle Lidia L Esposito Giovanni G Ghisi Margherita M Curtarello Matteo M Bonanno Laura L Masiero Massimo M Ribatti Domenico D Stürzl Michael M Naschberger Elisabeth E Croner Roland S RS Jubb Adrian M AM Harris Adrian L AL Koeppen Hartmut H Amadori Alberto A Indraccolo Stefano S

The Journal of pathology 20110519 4

Increased Notch1 activity has been observed in intestinal tumours, partially accomplished by β-catenin-mediated up-regulation of the Notch ligand Jagged-1. Whether further mechanisms of Notch activation exist and other Notch receptors might be involved is unclear. Microarray data indicated that Notch3 transcript levels are significantly up-regulated in primary and metastatic CRC samples compared to normal mucosa. Moreover, Notch3 protein was expressed at strong/moderate levels by 19.7% of 158 CR ...[more]

PMID: 21598247

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Project description:SMARD1 is an infantile autosomal recessive motor neuron (MN) disease, caused by mutations in the Immunoglobulin mu binding protein 2 (IGHMBP2). We investigated the potential of a spinal cord neural stem cell population isolated on the basis of aldehyde dehydrogenase activity (ALDH) to modify disease progression of nmd mice, an animal model of SMARD1. ALDHhiSSClo stem cells are self-renewing and multipotent and when intratechally transplanted in nmd mice generate motor neurons properly localized in the spinal cord ventral horns. Transplanted nmd animals presented delayed disease progression, sparing of motor neurons and ventral root axons and increased life-span. To further investigate the molecular events responsible for these differences, microarray and Real time RT-PCR analysis of wild-type, mutated and transplanted nmd spinal cord were undertaken. We demonstrated a down-regulation of genes involved in excitatory amino acid toxicity and oxidative stress handling, as well as an up-regulation of genes related to the chromatin organization in nmd compared to wild-type mice, suggesting that they may play a role in SMARD1 pathogenesis. Spinal cord of nmd transplanted mice expressed high transcript levels for genes related to neurogenesis such as Doublecortin (DCX), LIS1 and drebrin. The presence of DCX-expressing cells in adult nmd spinal cord suggests that both exogenous and endogenous neurogenesis may contribute to the observed nmd phenotype amelioration. Experiment Overall Design: We intratechally transplanted a spinal cord neural stem cell population isolated on the basis of aldehyde dehydrogenase activity (ALDH) in nmd mice, an animal model of SMARD1. Experiment Overall Design: We analyzed the lumbar spinal cord tract of transplanted nmd mice (n=3), untransplanted nmd mice (n=3) and wild-type mice (n=3) (all mice are of male gender). The latter groups underwent surgical procedure with vehicle. The surgical procedure and cell transplantation were done at P1 and the animals were sacrificed at 6 weeks of age.

Dataset Information

Indraccolo_Notch3

Publications

Notch3 signalling promotes tumour growth in colorectal cancer.

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