2000 Fiscal Year Final Research Report Summary
Molecular analysis of key factors involved in the mechanism of invasion in gliomas
| Project/Area Number |
09671448
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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 |
Cerebral neurosurgery
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| Research Institution | KEIO UNIVERSITY |
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Principal Investigator |
YOSHIDA Kazunari Keio Univ., School of Medicine, Assistant Professor, 医学部, 講師 (70166940)
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| Co-Investigator(Kenkyū-buntansha) |
KATAYAMA Makoto Keio Univ., School of Medicine, Assistant, 医学部, 助手 (90286493)
ISHIMORI Hisatugu Keio Univ., School of Medicine, Assistant, 医学部, 助手 (30286489)
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| Project Period (FY) |
1997 – 2000
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| Keywords | Glioma / malignant / c-Met protein / Invasion / NCAM / Musashi / NGF |
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| Research Abstract |
The malignant behavior of glioma is characterized by its invasiveness and its biological mechanism is of significant interest among scientists, Key factors contributing to its biology is yet to be determined. Hepatocyte growth factor (HGF) which has various physiological functions, and its receptor c-Met are thought to be determinant in the pathological processes of various malignancies. Concominant expression of HGF and c-met genes has been reported in glioma cell lines but little is known about the characteristics in glioma tissue. We made an analysis to elucidate the function of c-Met in glioma tissues which are concluded that 1) cultured astrocytes express c-Met protein and, 2) various neurotropic factors elevate the expression of NGF, 3) expression of c-Met protein interrelates with the recurrence of low-grade astrocytomas, and interrelation with the mechanism of invasion of glioma and not the malignant progression.
Cell adhesion molecules are also among the key factors of the malignant potential of brain tumors. Evidence from usage of glioma cell lines has shown correlation of neural cell adhesion molecule (NCAM) with the migratory and invasive potential nature. He studied the expression of NCAM in astrocytic tumors which elucidated that each NCAM isoform decreased its proportion to the progression of the histological malignancy. In other words, reduced NCAM expression might result in development of biological malignancy. We also ascertained the expression and the relation of Musashi expression which is known as a key factor in maturation of the neural stem cell.
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