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Stromal cell‐derived factor‐1α‐induced cell proliferation and its possible regulation by CD26/dipeptidyl peptidase IV in endometrial adenocarcinoma
Author(s) -
Mizokami Yayoi,
Kajiyama Hiroaki,
Shibata Kiyosumi,
Ino Kazuhiko,
Kikkawa Fumitaka,
Mizutani Shigehiko
Publication year - 2004
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.20183
Subject(s) - stromal cell , dipeptidyl peptidase , transfection , cell growth , cancer research , dipeptidyl peptidase 4 , biology , cell culture , cxcr4 , cell , microbiology and biotechnology , medicine , endocrinology , receptor , chemokine , biochemistry , enzyme , genetics , diabetes mellitus , type 2 diabetes
CD26/dipeptidylpeptidase IV (DPPIV) is a 110 kD membrane‐bound extracellular peptidase with ubiquitous expressions, and has a variety of functional properties in the development of human malignancies as well as T‐cell biology. According to recent reports, stromal cell derived factor‐1α (SDF‐1α), which is a good substrate for CD26/DPPIV, is expressed in various solid tumors and is involved in tumor development or metastasis. We investigated the expression of SDF‐1α and its corresponding receptor, CXCR4, in human endometrial carcinoma (EMCA) tissues and the function of SDF‐1α on EMCA cells with its regulation by CD26/DPPIV. We demonstrated that SDF‐1α and CXCR4 were expressed in human EMCA, and these immunoreactivities were significantly low in Grade 3 EMCA, which was similar to that of CD26/DPPIV, compared to those in Grade 1 and Grade 2. Additionally, exogenous SDF‐1α concentration was significantly lower in CD26/DPPIV‐transfected EMCA cells than that in vector‐transfected cells. Moreover, exogenous SDF‐1α significantly stimulated cell proliferation in vector‐transfected cells in a concentration dependent manner. In contrast, in CD26/DPPIV‐transfected cells, there was no apparent effect on proliferation shown by the addition of exogenous SDF‐1α. This is the first report showing a direct link between the SDF‐1α/CXCR4 pathway with CD26/DPPIV in solid tumors, suggesting that CD26/DPPIV is likely to directly modulate various SDF‐1α induced functions. © 2004 Wiley‐Liss, Inc.

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