Overexpression of wild-type PKD2 leads to increased proliferation and invasion of BON endocrine cells

Lindsey N. Jackson, Jing Li, L. Andy Chen, Courtney Townsend, B. Mark Evers

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

Carcinoid tumors are rare neuroendocrine tumors with a predilection for the gastrointestinal tract. Protein kinase D (PKD), a novel serine/threonine protein kinase, has been implicated in the regulation of transport processes in certain cell types. We have reported an important role for PKD in stimulated peptide secretion from a human (BON) carcinoid cell line; however, the role of PKD isoforms, including PKD2, in the proliferation and invasion of carcinoid tumors remains unclear. In the present study, we found that overexpression of PKD2 by stable transfection of BON cells with PKD2-wild type (PKD2WT) significantly increased proliferation and invasion compared to cells transfected with PKD2-kinase dead (PKD2KD) or pcDNA3 (control). Similarly, inhibition of PKD2 activity with small interfering RNA (siRNA) significantly decreased proliferation and invasion compared to cells transfected with non-targeting control (NTC) siRNA. These data support an important role for PKD2 in carcinoid tumor progression. Targeted inhibition of the PKD family may prove to be a novel treatment option for patients with carcinoid tumors.

Original languageEnglish (US)
Pages (from-to)945-949
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume348
Issue number3
DOIs
StatePublished - Sep 29 2006

    Fingerprint

Keywords

  • BON cell line
  • Carcinoid
  • Neuroendocrine
  • Protein kinase D2 (PKD2)
  • Small interfering RNA (siRNA)

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this