Loss of 14-3-3σ in Prostate Cancer and Its Precursors

Liang Cheng, Chong-Xian Pan, Jian Ting Zhang, Shaobo Zhang, Michael S. Kinch, Lang Li, Lee Ann Baldridge, Christopher Wade, Zhiqiang Hu, Michael O. Koch, Thomas M. Ulbright, John N. Eble

Research output: Contribution to journalArticle

81 Citations (Scopus)

Abstract

Purpose: The 14-3-3 family proteins are highly conserved over many mammalian species. The σ isoform (also called HME-1 or stratifin) is expressed in epithelial cells. Loss of 14-3-3σ is associated with failure to arrest the cell cycle at the G2-M phase checkpoint after DNA damage that leads to increased G2-type chromosomal aberrations. The role of 14-3-3σ in prostatic carcinogenesis is uncertain. Experimental Design: We studied one hundred and eleven specimens of invasive prostate adenocarcinoma with paired, adjacent high-grade prostatic intraepithelial neoplasia and normal prostate epithelium. Immunohistochemistry was used to detect the expression of 14-3-3σ. The findings were correlated with various clinical pathological parameters. Results: 14-3-3σ is ubiquitously expressed at high levels in normal prostate epithelium. Its expression is significantly decreased in prostatic intraepithelial neoplasia and prostatic adenocarcinoma. Ninety percent of samples of prostatic intraepithelial neoplasia had no or low 14-3-3σ expression. Ninety-seven percent of invasive adenocarcinomas had no or low 14-3-3σ expression. In most specimens (90%), suppression of 14-3-3σ expression occurred during the development of prostatic intraepithelial neoplasia from normal epithelium. Conclusions: Our data suggest that loss of 14-3-3σ contributes to the development of prostate adenocarcinoma. 14-3-3σ expression is significantly decreased during the progression of normal prostatic epithelium to prostatic intraepithelial neoplasia and invasive cancer.

Original languageEnglish (US)
Pages (from-to)3064-3068
Number of pages5
JournalClinical Cancer Research
Volume10
Issue number9
DOIs
StatePublished - May 1 2004
Externally publishedYes

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Prostatic Intraepithelial Neoplasia
Prostatic Neoplasms
Prostate
Adenocarcinoma
Epithelium
G2 Phase Cell Cycle Checkpoints
M Phase Cell Cycle Checkpoints
14-3-3 Proteins
Cell Cycle Checkpoints
Chromosome Aberrations
DNA Damage
Protein Isoforms
Carcinogenesis
Research Design
Epithelial Cells
Immunohistochemistry
Neoplasms

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Cheng, L., Pan, C-X., Zhang, J. T., Zhang, S., Kinch, M. S., Li, L., ... Eble, J. N. (2004). Loss of 14-3-3σ in Prostate Cancer and Its Precursors. Clinical Cancer Research, 10(9), 3064-3068. https://doi.org/10.1158/1078-0432.CCR-03-0652

Loss of 14-3-3σ in Prostate Cancer and Its Precursors. / Cheng, Liang; Pan, Chong-Xian; Zhang, Jian Ting; Zhang, Shaobo; Kinch, Michael S.; Li, Lang; Baldridge, Lee Ann; Wade, Christopher; Hu, Zhiqiang; Koch, Michael O.; Ulbright, Thomas M.; Eble, John N.

In: Clinical Cancer Research, Vol. 10, No. 9, 01.05.2004, p. 3064-3068.

Research output: Contribution to journalArticle

Cheng, L, Pan, C-X, Zhang, JT, Zhang, S, Kinch, MS, Li, L, Baldridge, LA, Wade, C, Hu, Z, Koch, MO, Ulbright, TM & Eble, JN 2004, 'Loss of 14-3-3σ in Prostate Cancer and Its Precursors', Clinical Cancer Research, vol. 10, no. 9, pp. 3064-3068. https://doi.org/10.1158/1078-0432.CCR-03-0652
Cheng, Liang ; Pan, Chong-Xian ; Zhang, Jian Ting ; Zhang, Shaobo ; Kinch, Michael S. ; Li, Lang ; Baldridge, Lee Ann ; Wade, Christopher ; Hu, Zhiqiang ; Koch, Michael O. ; Ulbright, Thomas M. ; Eble, John N. / Loss of 14-3-3σ in Prostate Cancer and Its Precursors. In: Clinical Cancer Research. 2004 ; Vol. 10, No. 9. pp. 3064-3068.
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AU - Pan, Chong-Xian

AU - Zhang, Jian Ting

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AU - Kinch, Michael S.

AU - Li, Lang

AU - Baldridge, Lee Ann

AU - Wade, Christopher

AU - Hu, Zhiqiang

AU - Koch, Michael O.

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N2 - Purpose: The 14-3-3 family proteins are highly conserved over many mammalian species. The σ isoform (also called HME-1 or stratifin) is expressed in epithelial cells. Loss of 14-3-3σ is associated with failure to arrest the cell cycle at the G2-M phase checkpoint after DNA damage that leads to increased G2-type chromosomal aberrations. The role of 14-3-3σ in prostatic carcinogenesis is uncertain. Experimental Design: We studied one hundred and eleven specimens of invasive prostate adenocarcinoma with paired, adjacent high-grade prostatic intraepithelial neoplasia and normal prostate epithelium. Immunohistochemistry was used to detect the expression of 14-3-3σ. The findings were correlated with various clinical pathological parameters. Results: 14-3-3σ is ubiquitously expressed at high levels in normal prostate epithelium. Its expression is significantly decreased in prostatic intraepithelial neoplasia and prostatic adenocarcinoma. Ninety percent of samples of prostatic intraepithelial neoplasia had no or low 14-3-3σ expression. Ninety-seven percent of invasive adenocarcinomas had no or low 14-3-3σ expression. In most specimens (90%), suppression of 14-3-3σ expression occurred during the development of prostatic intraepithelial neoplasia from normal epithelium. Conclusions: Our data suggest that loss of 14-3-3σ contributes to the development of prostate adenocarcinoma. 14-3-3σ expression is significantly decreased during the progression of normal prostatic epithelium to prostatic intraepithelial neoplasia and invasive cancer.

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