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Article: Tumor protein 53-induced nuclear protein 1 expression is repressed by miR-155, and its restoration inhibits pancreatic tumor development
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TitleTumor protein 53-induced nuclear protein 1 expression is repressed by miR-155, and its restoration inhibits pancreatic tumor development
 
AuthorsGironella, M1 4
Seux, M1 4
Xie, MJ4
Cano, C1 4
Tomasini, R1 4
Gommeaux, J1 4
Garcia, S1 4
Nowak, J1 4
Yeung, ML5
Jeang, KT5
Chaix, A1 4
Fazli, L6
Motoo, Y2
Wang, Q4
Rocchi, P1 4
Russo, A3
Gleave, M6
Dagorn, JC1 4
Iovanna, JL1 4
Carrier, A1 4
Pébusque, MJ1 4
Dusetti, NJ1 4
 
Issue Date2007
 
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
 
CitationProceedings Of The National Academy Of Sciences Of The United States Of America, 2007, v. 104 n. 41, p. 16170-16175 [How to Cite?]
DOI: http://dx.doi.org/10.1073/pnas.0703942104
 
AbstractPancreatic cancer is a disease with an extremely poor prognosis. Tumor protein 53-induced nuclear protein 1 (TP53INP1) is a proapoptotic stress-induced p53 target gene. In this article, we show by immunohistochemical analysis that TP53INP1 expression is dramatically reduced in pancreatic ductal adenocarcinoma (PDAC) and this decrease occurs early during pancreatic cancer development. TP53INP1 reexpression in the pancreatic cancer-derived cell line MiaPaCa2 strongly reduced its capacity to form s.c., i.p., and intrapancreatic tumors in nude mice. This anti-tumoral capacity is, at least in part, due to the induction of caspase 3-mediated apoptosis. In addition, TP53INP1 -/- mouse embryonic fibroblasts (MEFs) transformed with a retrovirus expressing E1A/ras V12 oncoproteins developed bigger tumors than TP53INP1 +/+ transformed MEFs or TP53INP1 -/- transformed MEFs with restored TP53INP1 expression. Finally, TP53INP1 expression is repressed by the oncogenic micro RNA miR-155, which is overexpressed in PDAC cells. TP53INP1 is a previously unknown miR-155 target presenting anti-tumoral activity. © 2007 by The National Academy of Sciences of the USA.
 
ISSN0027-8424
2013 Impact Factor: 9.809
 
DOIhttp://dx.doi.org/10.1073/pnas.0703942104
 
ISI Accession Number IDWOS:000250128800037
 
DC FieldValue
dc.contributor.authorGironella, M
 
dc.contributor.authorSeux, M
 
dc.contributor.authorXie, MJ
 
dc.contributor.authorCano, C
 
dc.contributor.authorTomasini, R
 
dc.contributor.authorGommeaux, J
 
dc.contributor.authorGarcia, S
 
dc.contributor.authorNowak, J
 
dc.contributor.authorYeung, ML
 
dc.contributor.authorJeang, KT
 
dc.contributor.authorChaix, A
 
dc.contributor.authorFazli, L
 
dc.contributor.authorMotoo, Y
 
dc.contributor.authorWang, Q
 
dc.contributor.authorRocchi, P
 
dc.contributor.authorRusso, A
 
dc.contributor.authorGleave, M
 
dc.contributor.authorDagorn, JC
 
dc.contributor.authorIovanna, JL
 
dc.contributor.authorCarrier, A
 
dc.contributor.authorPébusque, MJ
 
dc.contributor.authorDusetti, NJ
 
dc.date.accessioned2012-07-12T01:51:56Z
 
dc.date.available2012-07-12T01:51:56Z
 
dc.date.issued2007
 
dc.description.abstractPancreatic cancer is a disease with an extremely poor prognosis. Tumor protein 53-induced nuclear protein 1 (TP53INP1) is a proapoptotic stress-induced p53 target gene. In this article, we show by immunohistochemical analysis that TP53INP1 expression is dramatically reduced in pancreatic ductal adenocarcinoma (PDAC) and this decrease occurs early during pancreatic cancer development. TP53INP1 reexpression in the pancreatic cancer-derived cell line MiaPaCa2 strongly reduced its capacity to form s.c., i.p., and intrapancreatic tumors in nude mice. This anti-tumoral capacity is, at least in part, due to the induction of caspase 3-mediated apoptosis. In addition, TP53INP1 -/- mouse embryonic fibroblasts (MEFs) transformed with a retrovirus expressing E1A/ras V12 oncoproteins developed bigger tumors than TP53INP1 +/+ transformed MEFs or TP53INP1 -/- transformed MEFs with restored TP53INP1 expression. Finally, TP53INP1 expression is repressed by the oncogenic micro RNA miR-155, which is overexpressed in PDAC cells. TP53INP1 is a previously unknown miR-155 target presenting anti-tumoral activity. © 2007 by The National Academy of Sciences of the USA.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 2007, v. 104 n. 41, p. 16170-16175 [How to Cite?]
DOI: http://dx.doi.org/10.1073/pnas.0703942104
 
dc.identifier.citeulike2795096
 
dc.identifier.doihttp://dx.doi.org/10.1073/pnas.0703942104
 
dc.identifier.epage16175
 
dc.identifier.isiWOS:000250128800037
 
dc.identifier.issn0027-8424
2013 Impact Factor: 9.809
 
dc.identifier.issue41
 
dc.identifier.pmid17911264
 
dc.identifier.scopuseid_2-s2.0-36048952786
 
dc.identifier.spage16170
 
dc.identifier.urihttp://hdl.handle.net/10722/152576
 
dc.identifier.volume104
 
dc.languageeng
 
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
 
dc.publisher.placeUnited States
 
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of America
 
dc.titleTumor protein 53-induced nuclear protein 1 expression is repressed by miR-155, and its restoration inhibits pancreatic tumor development
 
dc.typeArticle
 
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<contributor.author>Tomasini, R</contributor.author>
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Author Affiliations
  1. Aix Marseille Université
  2. Kanazawa Medical University
  3. Università degli Studi di Palermo
  4. Inserm
  5. National Institute of Allergy and Infectious Diseases
  6. Vancouver General Hospital