Overexpression and knock-down studies highlight that a disintegrin and metalloproteinase 28 controls proliferation and migration in human prostate cancer

C. Rudnicka, S. Mochizuki, Y. Okada, C. McLaughlin, Peter J. Leedman, Lisa Stuart, Michael Epis, G. Hoyne, S. Boulos, Liam Johnson, Markus Schlaich, Vance Matthews

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

© 2016 the Author(s). Published by Wolters Kluwer Health, Inc. All rights reserved.Prostate cancer is one of the most prevalent cancers inmen. It is critical to identify and characterize oncogenes that drive the pathogenesis of human prostate cancer. The current study builds upon previous research showing that a disintegrin and metallproteinase (ADAM)28 is involved in the pathogenesis of numerous cancers. Our novel study used overexpression, pharmacological, and molecular approaches to investigate the biological function of ADAM28 in human prostate cancer cells,with a focus on cell proliferation andmigration. The results of this study provide important insights into the role of metalloproteinases in human prostate cancer. The expression of ADAM28 protein levels was assessed within human prostate tumors and normal adjacent tissue by immunohistochemistry. Immunocytochemistry and western blotting were used to assess ADAM28 protein expression in human prostate cancer cell lines. Functional assays were conducted to assess proliferation and migration in human prostate cancer cells in which ADAM28 protein expression or activity had been altered by overexpression, pharmacological inhibition, or by siRNA gene knockdown. The membrane bound ADAM28 was increased in human tumor biopsies and prostate cancer cell lines. Pharmacological inhibition of ADAM28 activity and/or knockdown of ADAM28 significantly reduced proliferation and migration of human prostate cancer cells, while overexpression of ADAM28 significantly increased proliferation and migration. ADAM28 is overexpressed in primary human prostate tumor biopsies, and it promotes human prostate cancer cell proliferation and migration. This study supports the notion that inhibition of ADAM28 may be a potential novel therapeutic strategy for human prostate cancer.
Original languageEnglish
Pages (from-to)1-8
Number of pages8
JournalMedicine (United States)
Volume95
Issue number40
DOIs
Publication statusPublished - 2016

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Disintegrins
Metalloproteases
Prostatic Neoplasms
Pharmacology
Neoplasms
Prostate
Immunohistochemistry
Cell Proliferation
Gene Knockdown Techniques
Biopsy
Cell Line
Proteins
Oncogenes
Small Interfering RNA
Cell Movement
Western Blotting

Cite this

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title = "Overexpression and knock-down studies highlight that a disintegrin and metalloproteinase 28 controls proliferation and migration in human prostate cancer",
abstract = "{\circledC} 2016 the Author(s). Published by Wolters Kluwer Health, Inc. All rights reserved.Prostate cancer is one of the most prevalent cancers inmen. It is critical to identify and characterize oncogenes that drive the pathogenesis of human prostate cancer. The current study builds upon previous research showing that a disintegrin and metallproteinase (ADAM)28 is involved in the pathogenesis of numerous cancers. Our novel study used overexpression, pharmacological, and molecular approaches to investigate the biological function of ADAM28 in human prostate cancer cells,with a focus on cell proliferation andmigration. The results of this study provide important insights into the role of metalloproteinases in human prostate cancer. The expression of ADAM28 protein levels was assessed within human prostate tumors and normal adjacent tissue by immunohistochemistry. Immunocytochemistry and western blotting were used to assess ADAM28 protein expression in human prostate cancer cell lines. Functional assays were conducted to assess proliferation and migration in human prostate cancer cells in which ADAM28 protein expression or activity had been altered by overexpression, pharmacological inhibition, or by siRNA gene knockdown. The membrane bound ADAM28 was increased in human tumor biopsies and prostate cancer cell lines. Pharmacological inhibition of ADAM28 activity and/or knockdown of ADAM28 significantly reduced proliferation and migration of human prostate cancer cells, while overexpression of ADAM28 significantly increased proliferation and migration. ADAM28 is overexpressed in primary human prostate tumor biopsies, and it promotes human prostate cancer cell proliferation and migration. This study supports the notion that inhibition of ADAM28 may be a potential novel therapeutic strategy for human prostate cancer.",
author = "C. Rudnicka and S. Mochizuki and Y. Okada and C. McLaughlin and Leedman, {Peter J.} and Lisa Stuart and Michael Epis and G. Hoyne and S. Boulos and Liam Johnson and Markus Schlaich and Vance Matthews",
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doi = "10.1097/MD.0000000000005085",
language = "English",
volume = "95",
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}

Overexpression and knock-down studies highlight that a disintegrin and metalloproteinase 28 controls proliferation and migration in human prostate cancer. / Rudnicka, C.; Mochizuki, S.; Okada, Y.; McLaughlin, C.; Leedman, Peter J.; Stuart, Lisa; Epis, Michael; Hoyne, G.; Boulos, S.; Johnson, Liam; Schlaich, Markus; Matthews, Vance.

In: Medicine (United States), Vol. 95, No. 40, 2016, p. 1-8.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Overexpression and knock-down studies highlight that a disintegrin and metalloproteinase 28 controls proliferation and migration in human prostate cancer

AU - Rudnicka, C.

AU - Mochizuki, S.

AU - Okada, Y.

AU - McLaughlin, C.

AU - Leedman, Peter J.

AU - Stuart, Lisa

AU - Epis, Michael

AU - Hoyne, G.

AU - Boulos, S.

AU - Johnson, Liam

AU - Schlaich, Markus

AU - Matthews, Vance

PY - 2016

Y1 - 2016

N2 - © 2016 the Author(s). Published by Wolters Kluwer Health, Inc. All rights reserved.Prostate cancer is one of the most prevalent cancers inmen. It is critical to identify and characterize oncogenes that drive the pathogenesis of human prostate cancer. The current study builds upon previous research showing that a disintegrin and metallproteinase (ADAM)28 is involved in the pathogenesis of numerous cancers. Our novel study used overexpression, pharmacological, and molecular approaches to investigate the biological function of ADAM28 in human prostate cancer cells,with a focus on cell proliferation andmigration. The results of this study provide important insights into the role of metalloproteinases in human prostate cancer. The expression of ADAM28 protein levels was assessed within human prostate tumors and normal adjacent tissue by immunohistochemistry. Immunocytochemistry and western blotting were used to assess ADAM28 protein expression in human prostate cancer cell lines. Functional assays were conducted to assess proliferation and migration in human prostate cancer cells in which ADAM28 protein expression or activity had been altered by overexpression, pharmacological inhibition, or by siRNA gene knockdown. The membrane bound ADAM28 was increased in human tumor biopsies and prostate cancer cell lines. Pharmacological inhibition of ADAM28 activity and/or knockdown of ADAM28 significantly reduced proliferation and migration of human prostate cancer cells, while overexpression of ADAM28 significantly increased proliferation and migration. ADAM28 is overexpressed in primary human prostate tumor biopsies, and it promotes human prostate cancer cell proliferation and migration. This study supports the notion that inhibition of ADAM28 may be a potential novel therapeutic strategy for human prostate cancer.

AB - © 2016 the Author(s). Published by Wolters Kluwer Health, Inc. All rights reserved.Prostate cancer is one of the most prevalent cancers inmen. It is critical to identify and characterize oncogenes that drive the pathogenesis of human prostate cancer. The current study builds upon previous research showing that a disintegrin and metallproteinase (ADAM)28 is involved in the pathogenesis of numerous cancers. Our novel study used overexpression, pharmacological, and molecular approaches to investigate the biological function of ADAM28 in human prostate cancer cells,with a focus on cell proliferation andmigration. The results of this study provide important insights into the role of metalloproteinases in human prostate cancer. The expression of ADAM28 protein levels was assessed within human prostate tumors and normal adjacent tissue by immunohistochemistry. Immunocytochemistry and western blotting were used to assess ADAM28 protein expression in human prostate cancer cell lines. Functional assays were conducted to assess proliferation and migration in human prostate cancer cells in which ADAM28 protein expression or activity had been altered by overexpression, pharmacological inhibition, or by siRNA gene knockdown. The membrane bound ADAM28 was increased in human tumor biopsies and prostate cancer cell lines. Pharmacological inhibition of ADAM28 activity and/or knockdown of ADAM28 significantly reduced proliferation and migration of human prostate cancer cells, while overexpression of ADAM28 significantly increased proliferation and migration. ADAM28 is overexpressed in primary human prostate tumor biopsies, and it promotes human prostate cancer cell proliferation and migration. This study supports the notion that inhibition of ADAM28 may be a potential novel therapeutic strategy for human prostate cancer.

U2 - 10.1097/MD.0000000000005085

DO - 10.1097/MD.0000000000005085

M3 - Article

VL - 95

SP - 1

EP - 8

JO - Medicine (United States)

JF - Medicine (United States)

SN - 0025-7974

IS - 40

ER -