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sst2 Somatostatin Receptor Expression Reverses Tumorigenicity of Human Pancreatic Cancer Cells

Nathalie Delesque, Louis Buscail, Jean-Pierre Estève, Nathalie Saint-Laurent, Catherine Müller, Gisbert Weckbecker, Christian Bruns, Nicole Vaysse and Christiane Susini
Nathalie Delesque
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Louis Buscail
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Jean-Pierre Estève
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Nathalie Saint-Laurent
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Catherine Müller
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Gisbert Weckbecker
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Christian Bruns
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Nicole Vaysse
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Christiane Susini
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DOI:  Published March 1997
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Abstract

Among the five cloned somatostatin receptor subtypes (sst1 to sst5), sst2 mediates the antiproliferative effect of somatostatin analogues in vitro. Somatostatin analogues have been shown to inhibit cell growth in vitro and in vivo in pancreatic cancer models that expressed sst2. We recently demonstrated the loss of sst2 gene expression in human pancreatic adenocarcinomas and most of the derived pancreatic cancer cell lines. In the present study, we corrected the sst2 defect in human pancreatic cancer BxPC-3 and Capan-1 cells by stable transfection with human sst2 cDNA. In the absence of exogenous ligand, both BxPC-3 and Capan-1 cells expressing sst2 showed a significant reduction in cell growth. This inhibitory effect was blocked by treatment with antiserum to somatostatin. sst2-expressing cells produced somatostatin-like immunoreactivity that mainly corresponded to somatostatin 14, indicating the induction of a negative autocrine loop. In other respects, sst2 expression in Capan-1 cells induced a significant reduction of clonogenicity in soft agar. Moreover, a significantly reduced (Capan-1 cells) or suppressed (BxPC-3 cells) tumor growth in athymic nude mice was observed. The reversal of tumorigenicity induced by the restoration of sst2 expression suggests that the loss of sst2 contributes to the malignancy of human pancreatic cancers.

Footnotes

  • ↵1 Supported in part by Grant 6755 from the Association pour la Recherche contre le Cancer, Grant 9407556 from the Conseil Régional Midi Pyrénées, and a grant from the Institut de Recherche des Maladies de l'Appareil Digestif.

  • ↵2 To whom requests for reprints should be addressed, at Institut National de la Santé et de la Recherche Médicale U151, Institut Louis Bugnard, 1 avenue J. Poulhès, Bât L3. Centre Hospitalier Universitaire Rangueil 31054 Toulouse, Cédex, France. Phone: 33-5-61-32-24-07; Fax: 33-5-62-26-40-12; E-mail: Louis.Buscail@rangueil.inserm.fr.

  • Received September 4, 1996.
  • Accepted January 2, 1997.
  • ©1997 American Association for Cancer Research.
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March 1997
Volume 57, Issue 5
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sst2 Somatostatin Receptor Expression Reverses Tumorigenicity of Human Pancreatic Cancer Cells
Nathalie Delesque, Louis Buscail, Jean-Pierre Estève, Nathalie Saint-Laurent, Catherine Müller, Gisbert Weckbecker, Christian Bruns, Nicole Vaysse and Christiane Susini
Cancer Res March 1 1997 (57) (5) 956-962;

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sst2 Somatostatin Receptor Expression Reverses Tumorigenicity of Human Pancreatic Cancer Cells
Nathalie Delesque, Louis Buscail, Jean-Pierre Estève, Nathalie Saint-Laurent, Catherine Müller, Gisbert Weckbecker, Christian Bruns, Nicole Vaysse and Christiane Susini
Cancer Res March 1 1997 (57) (5) 956-962;
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