TY - JOUR
T1 - Overexpression of wild-type PKD2 leads to increased proliferation and invasion of BON endocrine cells
AU - Jackson, Lindsey N.
AU - Li, Jing
AU - Chen, L. Andy
AU - Townsend, Courtney M.
AU - Evers, B. Mark
N1 - Funding Information:
The authors thank Dr. Kathleen O’Connor for thoughtful comments, Zobeida Cruz-Monserrate for technical assistance, Emily Bayne and Andrea Ramirez for maintenance of the BON cell line, Karen Martin for manuscript preparation, and Tatsuo Uchida for statistical analysis. This work was supported by Grants R01DK48498, R37AG10885, P01DK35608, and T32DK07639 from the National Institutes of Health and a Jeane B. Kempner Scholar award (to L.N.J.).
PY - 2006/9/29
Y1 - 2006/9/29
N2 - 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.
AB - 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.
KW - BON cell line
KW - Carcinoid
KW - Neuroendocrine
KW - Protein kinase D2 (PKD2)
KW - Small interfering RNA (siRNA)
UR - http://www.scopus.com/inward/record.url?scp=33747194165&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2006.07.142
DO - 10.1016/j.bbrc.2006.07.142
M3 - Article
C2 - 16899224
AN - SCOPUS:33747194165
SN - 0006-291X
VL - 348
SP - 945
EP - 949
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -