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High mobility group protein HMGI(Y) enhances tumor cell growth, invasion, and matrix metalloproteinase‐2 expression in prostate cancer cells
Author(s) -
Takaha Natsuki,
Resar Linda M.S.,
Vindivich Don,
Coffey Donald S.
Publication year - 2004
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20049
Subject(s) - prostate cancer , cancer research , transfection , cell growth , cyr61 , biology , tissue inhibitor of metalloproteinase , cancer cell , gentamicin protection assay , cell culture , prostate , cancer , matrix metalloproteinase , medicine , metastasis , growth factor , receptor , genetics , ctgf
BACKGROUND The high mobility group protein HMGI(Y) has oncogenic properties and correlates with an aggressive phenotype in prostate cancer. The molecular mechanisms involved in transformation associated with HMGI(Y) overexpression remain unknown. METHODS The HMG‐I isoform was transfected and overexpressed in nonmetastatic Dunning prostate cancer cells (G cells) without detectable HMGI(Y). The assays of cell proliferation, tumor formation, in vitro invasion, and cDNA microarray were performed to assess the effect of HMGI(Y) overexpression in the transfected G cells. RESULTS Overexpression of HMG‐I in G cells significantly increases cell proliferation and tumor growth and also modestly enhances in vitro invasion compared to mock transfectant. cDNA microarray revealed that expression of the matrix metalloproteinase‐2 (MMP‐2) proform was increased eightfold in G cells overexpressing HMG‐I. CONCLUSIONS Overexpression of HMG‐I in prostate cancer cells enhances cell growth, invasion, and expression of the proform of MMP‐2, which may initiate early steps involved in the metastatic cascade. © 2004 Wiley‐Liss, Inc.