Analysis of the tumor cell-cell interaction in oral cancer invasion
Project/Area Number |
24592988
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Surgical dentistry
|
Research Institution | Hiroshima University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
TOBIUME Kei 広島大学, 大学院医歯薬保健学研究院, 准教授 (40350037)
HIGASHIKAWA Koichiro 広島大学, 病院, 講師 (80363084)
KAMATA Nobuyuki 広島大学, 医歯薬保健学研究院, 教授 (70242211)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 癌の浸潤 / EMT / 扁平上皮癌 / 口腔癌 / 癌の浸潤と転移 |
Outline of Final Research Achievements |
Oral cancer tissues generally show the invasion mass histopathologically. Various sized the invasion mass consists of canver cells which maintains cell-cell adhesion and progresses their growth into the submucosa. In this study, we invastigated the mechanism that invasion mass forms with EMT-dependent invasion system and non-EMT dependent EMT system via humoral factor. Humoral factors, CCN1(Cyr61) and galectin-1 which we newly found contributeed the interaction between EMT phenotype tumor cells and non-EMT phenotype tumor cells for the forming tumor invasion mass. This mechanism gives a new insight for the understanding of the local invasion of tumor and could come in useful for the blockage of tumor progression.
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Report
(4 results)
Research Products
(3 results)