CORE
🇺🇦
make metadata, not war
Services
Services overview
Explore all CORE services
Access to raw data
API
Dataset
FastSync
Content discovery
Recommender
Discovery
OAI identifiers
OAI Resolver
Managing content
Dashboard
Bespoke contracts
Consultancy services
Support us
Support us
Membership
Sponsorship
Community governance
Advisory Board
Board of supporters
Research network
About
About us
Our mission
Team
Blog
FAQs
Contact us
Secretory products from PC-3 and MCF-7 tumor cell lines upregulate osteopontin in MC3T3-E1 cells
Authors
Alemany
Bagley
+39 more
Ballard
Brennan
Brunetti
Buchkovich
Chen
Coolican
Edmondson
Engert
Florini
Fox
Groudine
Gu
Hasty
Heino
Kaliman
Kaliman
Kamikubo
Levine
Li
Lofquist
Malik
Martin
Molkentin
Murre
Musar�
Nabeshima
Nadal-Ginard
Pellizas
Rich
Rosenthal
Rotwein
Saitoh
Sambrook
Schneider
Silverman
Urban
Wolfe
Yamashita
Yoshizumi
Publication date
1 January 2000
Publisher
'Wiley'
Doi
Abstract
Tumor cells frequently have pronounced effects on the skeleton including bone destruction, bone pain, hypercalcemia, and depletion of bone marrow cells. Despite the serious sequelae associated with skeletal metastasis, the mechanisms by which tumor cells alter bone homeostasis remain largely unknown. In this study, we tested the hypothesis that the disruption of bone homeostasis by tumor cells is due in part to the ability of tumor cells to upregulate osteopontin (OPN) mRNA in osteoblasts. Conditioned media were collected from tumor cells that elicit either osteolytic (MCF-7, PC-3) or osteoblastic responses (LNCaP) in animal models and their effects on OPN gene expression were compared using an osteoblast precursor cell line, MC3T3-E1 cells. Secretory products from osteolytic but not osteoblastic tumor cell lines were demonstrated to upregulate OPN in osteoblasts while inhibiting osteoblast proliferation and differentiation. Signal transduction studies revealed that regulation of OPN was dependent on both protein kinase C (PKC) and the mitogen-activated protein (MAP) kinase cascade. These results suggest that the upregulation of OPN may play a key role in the development of osteolytic lesions. Furthermore, these results suggest that drugs that prevent activation of the MAP kinase pathway may be efficacious in the treatment of osteolytic metastases. J. Cell. Biochem. 78:607–616, 2000. © 2000 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/34901/1/10_ftp.pd
Similar works
Full text
Available Versions
Deep Blue Documents at the University of Michigan
See this paper in CORE
Go to the repository landing page
Download from data provider
oai:deepblue.lib.umich.edu:202...
Last time updated on 25/05/2012
Crossref
See this paper in CORE
Go to the repository landing page
Download from data provider
Last time updated on 24/08/2020