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IGF‐I secretion by prostate carcinoma cells does not alter tumor‐bone cell interactions in vitro or in vivo
Author(s) -
Rubin Janet,
Fan Xian,
Rahnert Jill,
Sen Buer,
Hsieh Chialing,
Murphy Tamara C.,
Nanes Mark S.,
Horton Lindsay G.,
Beamer Wesley G.,
Rosen Clifford J.
Publication year - 2006
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20379
Subject(s) - osteolysis , prostate cancer , osteoblast , in vivo , prostate , medicine , cancer research , pathology , carcinoma , bone metastasis , in vitro , cancer , endocrinology , biology , biochemistry , surgery , microbiology and biotechnology
BACKGROUND IGF‐I is an important growth and differentiative factor for osteoblasts and may have a role in defining prostate cancer risk and skeletal metastases. METHODS Conditioned media (CM) from human prostate cancer (PC), C4‐2 and C4‐2B, which produce osteoblastic lesions, and PC‐3, which causes osteolysis, was added to MC3T3‐E1 bone cultures. SCID mice were injected intratibially with these engineered cells. Tumor bearing tibiae were analyzed by microCT and pQCT. RESULTS CM from PC cells increased osteoblast proliferation and differentiation and was unaltered by the type of PC cell, IGF‐I antibodies, or exogenous IGF‐I and IGFBP2. Study of intratibial PC tumors in SCID mice showed that C4‐2 cells grew slowly preserving bone structure, while PC‐3 tumors caused rapid osteolysis. Overexpression of IGF‐I did not change either tumor progression or skeletal response. CONCLUSIONS IGF‐I is neither necessary nor sufficient for the osteoblastic response to PC metastases. Prostate © 2006 Wiley‐Liss, Inc.