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L1 augments cell migration and tumor growth but not β3 integrin expression in ovarian carcinomas
Author(s) -
Gast Daniela,
Riedle Svenja,
Riedle Svenja,
Schabath Heidi,
Schlich Sabine,
Schneider Annette,
Issa Yasmin,
Stoeck Alexander,
Fogel Mina,
Joumaa Safwan,
Wenger Till,
Herr Ingrid,
Gutwein Paul,
Altevogt Peter
Publication year - 2005
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.20869
Subject(s) - integrin , cancer research , cell growth , ovarian carcinomas , biology , ovarian cancer , pathology , cell , medicine , ovarian carcinoma , cancer , genetics
L1 is a neural cell adhesion molecule involved in cell migration, axon growth and guidance. Recent data have shown that L1 is overexpressed in ovarian and endometrial tumors and is associated with bad prognosis. How L1 promotes tumor progression is presently unknown. Here we show that L1 expression is predominantly confined to the invasive front of ovarian carcinomas. Overexpression of L1 in carcinoma cell lines by adenovirus‐mediated gene transfer enhanced the haptotactic cell migration on extracellular matrix proteins. Expression of L1 augmented tumor growth of carcinomas xenografted in nonobese diabetic/severe combined immunodeficient mice (NOD/SCID). A recent report has demonstrated L1‐dependent upregulation of β3 integrin involving activation of the extracellular signal‐regulated kinase (erk) pathway. We find that L1 and β3 integrin are not coexpressed in ovarian carcinoma tissues. Overexpression of L1 did not upregulate β3 integrin in ovarian carcinoma cell lines but could do so in HEK293 cells. Our results suggest that L1 could drive progression by enhancing cell migration and tumor growth but that L1 dependent and erk‐regulated gene expression requires cell‐type specific elements. © 2005 Wiley‐Liss, Inc.