2003 Fiscal Year Final Research Report Summary
Involvement of ras signal in the development of osteosarcoma
| Project/Area Number |
14571376
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
NAKAYAMA Tanitaka Kyoto University, Faculty of Medicine, assistant Professor, 医学研究科, 助手 (80335273)
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| Co-Investigator(Kenkyū-buntansha) |
TOGUCHIDA Junya Kyoto University, Institute for Frontier Medical Sciences, Professor, 再生医科学研究所, 教授 (40273502)
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| Project Period (FY) |
2002 – 2003
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| Keywords | osteosarcoma / ras / mesencymal stem cell |
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| Research Abstract |
Mesenchymal stem cell was immortalized by the induction of Bmi1 and teromerase genes. The immortalized cell line, hMSC-Bmi1-hT showed the abilities to differentiate into osteogenic, chondrogenic and adipogenic cell lineages, and no tumorigenic phenotype. Considering the cell as a precursor of osteosarcoma, we introduced the activated H-ras gene into the cell. The cell introduced by activatted H-ras gene showed vigorous proliferative activity even under low-serum culture condition, colony formation in soft agar, and tumorigenicity in the immunodeficient mice, eventually leading the mice to death. The tumors formed by the cell, however, showed no histologic features of osteosarcoma, such as the formation of osteoid. Result was the same when the H-ras gene was introduced after the hMSC-Bmi1-hT was induced the osteogenic differentiation. These results indicate the ras signaling is potentially involved in the neoplastic transformation in mesenchymal cells, and there is an unrevealed mechanism in the presentation of differentiated phenotype in mesenchymal tumor cells.
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