| Project/Area Number |
23590428
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | Yokohama City University |
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Principal Investigator |
OKUDELA KOJI 横浜市立大学, 医学部, 講師 (10326027)
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| Co-Investigator(Kenkyū-buntansha) |
KATAYA Akira 日本医科大学, 医学部, 助教 (10333113)
NAGAHARA Noriyuki 日本医科大学, 医学部, 准教授 (10208043)
WOO Tetsukan 横浜市立大学, 医学研究科, 共同研究員 (90537177)
YAZAWA Takuya 杏林大学, 医学部, 准教授 (50251054)
SHIMOYAMADA Hiroaki 杏林大学, 医学部, 助教 (60381472)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | atypism / lung cancer / 肺癌 / 異型性 / CLIC4 |
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| Research Abstract |
A purpose of present study is to elucidate a molecular basis of morphological atypism. This study investigated the proteome modulated by oncogenic KRAS in immortalized airway epithelial cells. We here focused on CLIC4 to investigate its potential involvement in an induction of the morphologic atypism in lung cancers. CILC4 protein levels were reduced in some lung cancer cell lines. The knockdown of CLIC4 in an immortalized airway cell line modulated a cell shape as marked enlargement of cells and nuclei. CLIC4 protein levels tended to be lower in high-grade tumors. These results suggest that the alteration in CLIC4 could induce some morphological atypism of neoplastic cells and could be involved in carcinogenesis of the lung.
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