Relationship between the membrane localization of D4GDI and the cancer progression in human colon cancer cells.
| Project/Area Number |
16591368
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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 |
Digestive surgery
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
MAEDA Masayo Kanazawa Med.Univ., School of Medicine, Assistant, 医学部, 助手 (30199632)
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| Co-Investigator(Kenkyū-buntansha) |
OTA Takahide Kanazawa Med.Univ., Med.Res.Inst., Associate Prof., 総合医学研究所, 助教授 (10152141)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2004: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | RhoGDI / LyGDI / D4GDI / RhoGDIβ / RhoGDI2 / metastasis / colon cancer / centrosome / tight function / cell division / polarity / D4GDI / Centrosome / Tight junction / RhoGDI2 / Rho / 細胞膜 / 細胞間接着 |
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| Research Abstract |
D4GDI (LyGDI/RhoGDIβ/RhoGDI2), which regulates the signaling pathways of Rho GTPases, localized at the tight junction of apical side of cell-cell interphase in a monolayer of MDCK cells and colon cancer cells which retained the epithelial morphology, but not in colon cancer cells which lost the epithelial morphology. Furthermore, D4GDI transiently localized to centrosomes in metaphase cells. These observations suggested that D4GDI played roles in the formation and/or maintenance of tight junction and in the cell division. To confirm such a possibility, we examined the phenotype of HeLa cells in which the expression of D4GDI was suppressed by siRNA more than 80%. The suppression of the expression of D4GDI increased the frequency of abnormally lobulated nuclei and the 8n and 16n cells, which were probably due to the aberrant cell division. These results confirmed that D4GDI participated in the regulation of cell division and cell polarity. D4GDI has been reported as metastasis suppressor. Our observations suggest that the decrease of the expression of D4GDI or the dysfunction of D4GDI give rise to the abnormal intercellular adhesion or the failure of cell division, thereby promote the progression of colon cancer.
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Report
(3 results)
Research Products
(8 results)
