Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/94378
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dc.contributor.author | Dorstyn, L. | - |
dc.contributor.author | Puccini, J. | - |
dc.contributor.author | Nikolic, A. | - |
dc.contributor.author | Shalini, S. | - |
dc.contributor.author | Wilson, C. | - |
dc.contributor.author | Norris, M. | - |
dc.contributor.author | Haber, M. | - |
dc.contributor.author | Kumar, S. | - |
dc.date.issued | 2014 | - |
dc.identifier.citation | Cell Death and Disease, 2014; 5(8):e1383-1-e1383-9 | - |
dc.identifier.issn | 2041-4889 | - |
dc.identifier.issn | 2041-4889 | - |
dc.identifier.uri | http://hdl.handle.net/2440/94378 | - |
dc.description.abstract | Caspase-2 has been implicated in various cellular functions, including cell death by apoptosis, oxidative stress response, maintenance of genomic stability and tumor suppression. The loss of the caspase-2 gene (Casp2) enhances oncogene-mediated tumorigenesis induced by E1A/Ras in athymic nude mice, and also in the Eμ-Myc lymphoma and MMTV/c-neu mammary tumor mouse models. To further investigate the function of caspase-2 in oncogene-mediated tumorigenesis, we extended our studies in the TH-MYCN transgenic mouse model of neuroblastoma. Surprisingly, we found that loss of caspase-2 delayed tumorigenesis in the TH-MYCN neuroblastoma model. In addition, tumors from TH-MYCN/Casp2(-/-) mice were predominantly thoracic paraspinal tumors and were less vascularized compared with tumors from their TH-MYCN/Casp2(+/+) counterparts. We did not detect any differences in the expression of neuroblastoma-associated genes in TH-MYCN/Casp2(-/-) tumors, or in the activation of Ras/MAPK signaling pathway that is involved in neuroblastoma progression. Analysis of expression array data from human neuroblastoma samples showed a correlation between low caspase-2 levels and increased survival. However, caspase-2 levels correlated with clinical outcome only in the subset of MYCN-non-amplified human neuroblastoma. These observations indicate that caspase-2 is not a suppressor in MYCN-induced neuroblastoma and suggest a tissue and context-specific role for caspase-2 in tumorigenesis. | - |
dc.description.statementofresponsibility | L Dorstyn, J Puccini, A Nikolic, S Shalini, CH Wilson, MD Norris, M Haber and S Kumar | - |
dc.language.iso | en | - |
dc.publisher | Nature | - |
dc.rights | Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/ | - |
dc.source.uri | http://dx.doi.org/10.1038/cddis.2014.342 | - |
dc.subject | Animals | - |
dc.subject | Mice, Inbred C57BL | - |
dc.subject | Mice, Transgenic | - |
dc.subject | Mice, Knockout | - |
dc.subject | Humans | - |
dc.subject | Mice | - |
dc.subject | Neuroblastoma | - |
dc.subject | Disease Models, Animal | - |
dc.subject | ras Proteins | - |
dc.subject | Mitogen-Activated Protein Kinases | - |
dc.subject | Signal Transduction | - |
dc.subject | Caspase 2 | - |
dc.subject | Kaplan-Meier Estimate | - |
dc.title | An unexpected role for caspase-2 in neuroblastoma | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1038/cddis.2014.342 | - |
dc.relation.grant | http://purl.org/au-research/grants/nhmrc/1043057 | - |
dc.relation.grant | http://purl.org/au-research/grants/nhmrc/1002863 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Kumar, S. [0000-0001-7126-9814] | - |
Appears in Collections: | Aurora harvest 2 Medicine publications |
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hdl_94378.pdf | Published version | 3.56 MB | Adobe PDF | View/Open |
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