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Differential expression of cytokines in rat osteosarcoma and malignant fibrous histiocytoma cell lines induced by 4‐(hydroxyamino)quinoline‐1‐oxide
Author(s) -
Honoki Kanya,
Tsujiuchi Toshifumi,
Sasaki Yasutaka,
Tsutsumi Masahiro,
Morishita Toru,
Kido Akira,
Miyauchi Yoshizumi,
Mii Yoshio,
Takakura Yoshinori,
Konishi Yoichi
Publication year - 2002
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.10021
Subject(s) - osteosarcoma , biology , transforming growth factor , cancer research , cell culture , cytokine , macrophage migration inhibitory factor , microbiology and biotechnology , immunology , genetics
Cytokines are considered to play an important role in tumor pathogenesis and progression, and recent studies have demonstrated that a variety of forms, including interleukins (ILs) and transforming growth factor‐βs (TGF‐βs), may regulate tumors. In the present study, the expression of TGF‐β isoforms and ILs was investigated in cell lines from a rat osteosarcoma and a malignant fibrous histiocytoma (MFH), both established from transplantable tumors induced by 4‐(hydroxyamino) quinoline 1‐oxide (4‐HAQO) in syngeneic F344 male rats. The results of a multiprobe RNase protection assay showed TGF‐β1 expression to be remarkably elevated, with no TGF‐β2 and β3 detectable in MFH cells, while TGF‐β1 and ‐β2 were found to be moderately and TGF‐β3 weakly expressed in osteosarcoma lines. All cell lines of osteosarcomas and MFHs expressed macrophage migration inhibitory factor at similar levels. In contrast to the lack of ILs in the MFH cells, moderate IL‐6 and very weak IL‐1β expression was detected in the osteosarcoma cells. These results suggest that variation in expression pattern of these cytokines in osteosarcomas and MFHs might be involved in differences in histological appearance and biological behavior, including metastatic ability, between these two mesenchyme‐derived tumor types. © 2002 Wiley‐Liss, Inc.