Inhibitory effects of transforming growth factor-beta1 pretreatment on experimental pulmonary metastasis of MCS-1 Chinese hamster mesenchymal chondrosarcoma cells
Recent studies have suggested that transforming growth factor(TGF)-beta1 acts as a multifunctional regulator of cell growth, and also modifies tumor progression and metastasis. In the present study, we investigated the effects of TGF-beta1 on the proliferation and experimental pulmonary metastasis o...
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Published in: | Tohoku journal of experimental medicine Vol. 187; no. 3; pp. 203 - 213 |
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Main Authors: | , , |
Format: | Journal Article |
Language: | English |
Published: |
Japan
1999
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Subjects: | |
Online Access: | Get full text |
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Summary: | Recent studies have suggested that transforming growth factor(TGF)-beta1 acts as a multifunctional regulator of cell growth, and also modifies tumor progression and metastasis. In the present study, we investigated the effects of TGF-beta1 on the proliferation and experimental pulmonary metastasis of MCS-1. MCS-1 are undifferentiated type cloned tumor cells established from a mesenchymal chondrosarcoma which spontaneously occurred in the soft tissue of a female Chinese hamster. MCS-1 cells were pretreated with TGF-beta1 (0, 0.05, 0.5, 2, 10 ng/ml) for 72 hours in a medium containing 1% fetal bovine serum, then tested for in vitro growth by the MTT method, in vivo growth by subcutaneous inoculation into athymic nude mice (1 x 10(6) cells/mouse) and experimental pulmonary metastasis by injection into the lateral tail vein of athymic nude mice (5 x 10(4) cells/mouse). TGF-beta1 significantly inhibited in vitro growth of MCS-1, depending on its concentrations, and also experimental metastasis with maximal inhibition at 0.5 or 2 ng/ml treatment compared to untreated controls. TGF-beta1, however, was ineffective for in vivo subcutaneous growth of MCS-1. These results indicated that TGF-beta1 might be an inhibitor of metastasis of mesenchymal chondrosarcomas including other types of non-epitherial cartilage or bone formation tumors. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0040-8727 1349-3329 |
DOI: | 10.1620/tjem.187.203 |