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WFRF:(Mattila Heikki)
 

Sökning: WFRF:(Mattila Heikki) > Mutant p53-associat...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004303naa a2200481 4500
001oai:DiVA.org:liu-106028
003SwePub
008140417s2014 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:128520714
024a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-1060282 URI
024a https://doi.org/10.1172/JCI672802 DOI
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1285207142 URI
040 a (SwePub)liud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Arjonen, Anttiu VTT Technical Research Centre Finland, Finland University of Turku, Finland4 aut
2451 0a Mutant p53-associated myosin-X upregulation promotes breast cancer invasion and metastasis
264 1b American Society for Clinical Investigation,c 2014
338 a print2 rdacarrier
520 a Mutations of the tumor suppressor TP53 are present in many forms of human cancer and are associated with increased tumor cell invasion and metastasis. Several mechanisms have been identified for promoting dissemination of cancer cells with TP53 mutations, including increased targeting of integrins to the plasma membrane. Here, we demonstrate a role for the filopodia-inducing motor protein Myosin-X (Myo10) in mutant p53-driven cancer invasion. Analysis of gene expression profiles from 2 breast cancer data sets revealed that MYO10 was highly expressed in aggressive cancer subtypes. Myo10 was required for breast cancer cell invasion and dissemination in multiple cancer cell lines and murine models of cancer metastasis. Evaluation of a Myo10 mutant without the integrin-binding domain revealed that the ability of Myo10 to transport 131 integrins to the filopodia tip is required for invasion. Introduction of mutant p53 promoted Myo10 expression in cancer cells and pancreatic ductal adenocarcinoma in mice, whereas suppression of endogenous mutant p53 attenuated Myo10 levels and cell invasion. In clinical breast carcinomas, Myo10 was predominantly expressed at the invasive edges and correlated with the presence of TP53 mutations and poor prognosis. These data indicate that Myo10 upregulation in mutant p53-driven cancers is necessary for invasion and that plasma-membrane protrusions, such as filopodia, may serve as specialized metastatic engines.
653 a MEDICINE
653 a MEDICIN
700a Kaukonen, Riinau VTT Technical Research Centre Finland, Finland University of Turku, Finland4 aut
700a Mattila, Elinau VTT Technical Research Centre Finland, Finland University of Turku, Finland4 aut
700a Rouhi, Pegahu Karolinska Institute, Sweden4 aut
700a Hognas, Gunillau VTT Technical Research Centre Finland, Finland University of Turku, Finland4 aut
700a Sihto, Harriu University of Helsinki, Finland4 aut
700a Miller, Bryan W.u University of Glasgow, Scotland4 aut
700a Morton, Jennifer P.u University of Glasgow, Scotland4 aut
700a Bucher, Elmaru VTT Technical Research Centre Finland, Finland4 aut
700a Taimen, Pekkau University of Turku, Finland Turku University Hospital, Finland4 aut
700a Virtakoivu, Reettau VTT Technical Research Centre Finland, Finland University of Turku, Finland4 aut
700a Cao, Yihaiu Karolinska Institutet,Linköpings universitet,Avdelningen för kardiovaskulär medicin,Hälsouniversitetet4 aut0 (Swepub:liu)yihca64
700a Sansom, Owen J.u University of Glasgow, Scotland4 aut
700a Joensuu, Heikkiu University of Helsinki, Finland University of Helsinki, Finland4 aut
700a Ivaska, Johannau VTT Technical Research Centre Finland, Finland University of Turku, Finland University of Turku, Finland4 aut
710a VTT Technical Research Centre Finland, Finland University of Turku, Finlandb Karolinska Institute, Sweden4 org
773t Journal of Clinical Investigationd : American Society for Clinical Investigationg 124:3, s. 1069-1082q 124:3<1069-1082x 0021-9738x 1558-8238
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-106028
8564 8u https://doi.org/10.1172/JCI67280
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:128520714

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