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

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

doi:10.1016/j.bbrc.2006.07.142

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

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

Research output: Contribution to journal › Article › peer-review

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 (PKD2_WT) significantly increased proliferation and invasion compared to cells transfected with PKD2-kinase dead (PKD2_KD) 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 language	English
Pages (from-to)	945-949
Number of pages	5
Journal	Biochemical and Biophysical Research Communications
Volume	348
Issue number	3
DOIs	https://doi.org/10.1016/j.bbrc.2006.07.142
State	Published - Sep 29 2006

Bibliographical note

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.).

Keywords

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

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/j.bbrc.2006.07.142

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title = "Overexpression of wild-type PKD2 leads to increased proliferation and invasion of BON endocrine cells",

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.",

keywords = "BON cell line, Carcinoid, Neuroendocrine, Protein kinase D2 (PKD2), Small interfering RNA (siRNA)",

author = "Jackson, {Lindsey N.} and Jing Li and Chen, {L. Andy} and Townsend, {Courtney M.} and Evers, {B. Mark}",

note = "Funding Information: The authors thank Dr. Kathleen O{\textquoteright}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.). ",

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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.

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

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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