pubmed-article:17506723 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17506723 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:17506723 | lifeskim:mentions | umls-concept:C0006118 | lld:lifeskim |
pubmed-article:17506723 | lifeskim:mentions | umls-concept:C0021641 | lld:lifeskim |
pubmed-article:17506723 | lifeskim:mentions | umls-concept:C0205282 | lld:lifeskim |
pubmed-article:17506723 | lifeskim:mentions | umls-concept:C0431085 | lld:lifeskim |
pubmed-article:17506723 | lifeskim:mentions | umls-concept:C0596138 | lld:lifeskim |
pubmed-article:17506723 | lifeskim:mentions | umls-concept:C0018284 | lld:lifeskim |
pubmed-article:17506723 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
pubmed-article:17506723 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
pubmed-article:17506723 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:17506723 | pubmed:dateCreated | 2007-7-24 | lld:pubmed |
pubmed-article:17506723 | pubmed:abstractText | AT/RTs (atypical teratoid/rhabdoid tumours) of the CNS (central nervous system) are childhood malignancies associated with poor survival rates due to resistance to conventional treatments such as chemotherapy. We characterized a panel of human AT/RT and MRT (malignant rhabdoid tumour) cell lines for expression of RTKs (receptor tyrosine kinases) and their involvement in tumour growth and survival. When compared with normal brain tissue, AT/RT cell lines overexpressed the IR (insulin receptor) and the IGFIR (insulin-like growth factor-I receptor). Moreover, insulin was secreted by AT/RT cells grown in serum-free medium. Insulin potently activated Akt (also called protein kinase B) in AT/RT cells, as compared with other growth factors, such as epidermal growth factor. Pharmacological inhibitors, neutralizing antibodies, or RNAi (RNA interference) targeting the IR impaired the growth of AT/RT cell lines and induced apoptosis. Inhibitors of the PI3K (phosphoinositide 3-kinase)/Akt pathway also impaired basal and insulin-stimulated AT/RT cell proliferation. Experiments using RNAi and isoform-specific pharmacological inhibitors established a key role for the class I(A) PI3K p110alpha isoform in AT/RT cell growth and insulin signalling. Taken together, our results reveal a novel role for autocrine signalling by insulin and the IR in growth and survival of malignant human CNS tumour cells via the PI3K/Akt pathway. | lld:pubmed |
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pubmed-article:17506723 | pubmed:language | eng | lld:pubmed |
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pubmed-article:17506723 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17506723 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17506723 | pubmed:month | Aug | lld:pubmed |
pubmed-article:17506723 | pubmed:issn | 1470-8728 | lld:pubmed |
pubmed-article:17506723 | pubmed:author | pubmed-author:JacksonShaun... | lld:pubmed |
pubmed-article:17506723 | pubmed:author | pubmed-author:ArcaroAlexand... | lld:pubmed |
pubmed-article:17506723 | pubmed:author | pubmed-author:Schoenwaelder... | lld:pubmed |
pubmed-article:17506723 | pubmed:author | pubmed-author:DelattreOlivi... | lld:pubmed |
pubmed-article:17506723 | pubmed:author | pubmed-author:FischerBarbar... | lld:pubmed |
pubmed-article:17506723 | pubmed:author | pubmed-author:GrotzerMichae... | lld:pubmed |
pubmed-article:17506723 | pubmed:author | pubmed-author:ShalabyTarekT | lld:pubmed |