1992 Fiscal Year Final Research Report Summary
Proliferation mechanism of protein-free culture
| Project/Area Number |
03670696
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Gunma University Medical School |
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Principal Investigator |
CHIGIRA Masaki Gunma University School of Medicine, Department of Orthopedic Surgery, Lecturer, 医学部, 講師 (70143196)
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| Co-Investigator(Kenkyū-buntansha) |
UDAGAWA Eiichi Gunma University School of Medicine, Department of Orthopedic Surgery, Professor, 医学部, 教授 (70009976)
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| Project Period (FY) |
1991 – 1992
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| Keywords | Protein-free culture / Autonomy / Calmodulin / Protein kinases / Inhibitors |
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| Research Abstract |
We hypothesized that autonomic proliferation of tumor cells is internally programmed a priori, autocrine growth hypothesis may not be suitable to the autonomy of tumor cells in vitro. According to this hypothesis, we demonstrated that endogenous proteins secreted into the medium by protein-free cells play a negative role in the proliferation of them in general. Addition of protein kinase C inhibitor to the protein-free culture enhanced proliferation of cells, although serum-dependent proliferation were inhibited at the same concentration. From these results, external signals which stimulate cell proliferation do not play a role in the protein-free culture, although the signals included autocrine growth factors and serum. On the other hand, inhibitors against calmodulin suppressed the proliferation of protein-free cells specifically. Immunoblotting for calmodulin revealed that nuclear content of calmodulin in protein-free cells were much higher than that of serum-dependent clones. Finally, our autonomic hypothesis of proliferation has been proved.
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Research Products
(14 results)
