Sökning: WFRF:(Mattila Heikki) > Mutant p53-associat...
Fältnamn | Indikatorer | Metadata |
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000 | 04303naa a2200481 4500 | |
001 | oai:DiVA.org:liu-106028 | |
003 | SwePub | |
008 | 140417s2014 | |||||||||||000 ||eng| | |
009 | oai:prod.swepub.kib.ki.se:128520714 | |
024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-1060282 URI |
024 | 7 | a https://doi.org/10.1172/JCI672802 DOI |
024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:1285207142 URI |
040 | a (SwePub)liud (SwePub)ki | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Arjonen, Anttiu VTT Technical Research Centre Finland, Finland University of Turku, Finland4 aut |
245 | 1 0 | a Mutant p53-associated myosin-X upregulation promotes breast cancer invasion and metastasis |
264 | 1 | b 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 | |
700 | 1 | a Kaukonen, Riinau VTT Technical Research Centre Finland, Finland University of Turku, Finland4 aut |
700 | 1 | a Mattila, Elinau VTT Technical Research Centre Finland, Finland University of Turku, Finland4 aut |
700 | 1 | a Rouhi, Pegahu Karolinska Institute, Sweden4 aut |
700 | 1 | a Hognas, Gunillau VTT Technical Research Centre Finland, Finland University of Turku, Finland4 aut |
700 | 1 | a Sihto, Harriu University of Helsinki, Finland4 aut |
700 | 1 | a Miller, Bryan W.u University of Glasgow, Scotland4 aut |
700 | 1 | a Morton, Jennifer P.u University of Glasgow, Scotland4 aut |
700 | 1 | a Bucher, Elmaru VTT Technical Research Centre Finland, Finland4 aut |
700 | 1 | a Taimen, Pekkau University of Turku, Finland Turku University Hospital, Finland4 aut |
700 | 1 | a Virtakoivu, Reettau VTT Technical Research Centre Finland, Finland University of Turku, Finland4 aut |
700 | 1 | a Cao, Yihaiu Karolinska Institutet,Linköpings universitet,Avdelningen för kardiovaskulär medicin,Hälsouniversitetet4 aut0 (Swepub:liu)yihca64 |
700 | 1 | a Sansom, Owen J.u University of Glasgow, Scotland4 aut |
700 | 1 | a Joensuu, Heikkiu University of Helsinki, Finland University of Helsinki, Finland4 aut |
700 | 1 | a Ivaska, Johannau VTT Technical Research Centre Finland, Finland University of Turku, Finland University of Turku, Finland4 aut |
710 | 2 | a VTT Technical Research Centre Finland, Finland University of Turku, Finlandb Karolinska Institute, Sweden4 org |
773 | 0 | t Journal of Clinical Investigationd : American Society for Clinical Investigationg 124:3, s. 1069-1082q 124:3<1069-1082x 0021-9738x 1558-8238 |
856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-106028 |
856 | 4 8 | u https://doi.org/10.1172/JCI67280 |
856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:128520714 |
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