The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
miR-380-5p represses p53 to control cellular survival and is associated with poor outcome in MYCN-amplified neuroblastoma
Open accessAbstract
Inactivation of the p53 tumor suppressor pathway allows cell survival in times of stress and occurs in many human cancers; however, normal embryonic stem cells and some cancers such as neuroblastoma maintain wild-type human TP53 and mouse Trp53 (referred to collectively as p53 herein). Here we describe a miRNA, miR-380-5p, that represses p53 expression via a conserved sequence in the p53 3′ untranslated region (UTR). miR-380-5p is highly expressed in mouse embryonic stem cells and neuroblastomas, and high expression correlates with poor outcome in neuroblastomas with neuroblastoma derived v-myc myelocytomatosis viral-related oncogene (MYCN) amplification. miR-380 overexpression cooperates with activated HRAS oncoprotein to transform primary cells, block oncogene-induced senescence and form tumors in mice. Conversely, inhibition of endogenous miR-380-5p in embryonic stem or neuroblastoma cells results in induction of p53, and extensive apoptotic cell death. In vivo delivery of a miR-380-5p antagonist decreases tumor size in an orthotopic mouse model of neuroblastoma. We demonstrate a new mechanism of p53 regulation in cancer and stem cells and uncover a potential therapeutic target for neuroblastoma.
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Metadata
- Authors
- Swarbrick, A., Woods, S. L., Shaw, A., Balakrishnan, A., Phua, Y., Nguyen, A., Chanthery, Y., Lim, L., Ashton, L. J., Judson, R. L., Huskey, N., Blelloch, R., Haber, M., Norris, M. D., Lengyel, P., Hackett, C. S., Preiss, T., Chetcuti, A., Sullivan, C. S., Marcusson, E. G., Weiss, W., L'Etoile, N., & Goga, A.
- Venue
- Nature Medicine
- Published
- 2010-09-26
- Volume
- 16
- Issue
- 10
- Pages
- 1134-1140
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2071689359
- Cited by
- 201
- References
- 11
- FWCI
- 5.06
- Type
- journal article
- Language
- en
- Open access
- green
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