High mobility group protein HMGI(Y) enhances tumor cell growth, invasion, and matrix metalloproteinase-2 expression in prostate cancer cells

Natsuki Takaha, Linda M Smith Resar, Don Vindivich, Donald S. Coffey

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)160-167
Number of pages8
JournalProstate
Volume60
Issue number2
DOIs
StatePublished - Jul 1 2004

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High Mobility Group Proteins
Gastrin-Secreting Cells
Matrix Metalloproteinase 2
Prostatic Neoplasms
Growth
Oligonucleotide Array Sequence Analysis
Neoplasms
Cell Proliferation
Protein Isoforms
Phenotype
In Vitro Techniques

Keywords

  • HMGI(Y)
  • Matrix metalloproteinase 2
  • Nuclear matrix
  • Prostate cancer

ASJC Scopus subject areas

  • Urology

Cite this

High mobility group protein HMGI(Y) enhances tumor cell growth, invasion, and matrix metalloproteinase-2 expression in prostate cancer cells. / Takaha, Natsuki; Smith Resar, Linda M; Vindivich, Don; Coffey, Donald S.

In: Prostate, Vol. 60, No. 2, 01.07.2004, p. 160-167.

Research output: Contribution to journalArticle

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abstract = "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.",
keywords = "HMGI(Y), Matrix metalloproteinase 2, Nuclear matrix, Prostate cancer",
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T1 - High mobility group protein HMGI(Y) enhances tumor cell growth, invasion, and matrix metalloproteinase-2 expression in prostate cancer cells

AU - Takaha, Natsuki

AU - Smith Resar, Linda M

AU - Vindivich, Don

AU - Coffey, Donald S.

PY - 2004/7/1

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N2 - 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.

AB - 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.

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