| Project/Area Number |
21790325
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Yokohama City University |
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Principal Investigator |
OKUDELA Koji Yokohama City University, 医学部, 助教 (10326027)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 異型性 / FXYD3 / 肺癌 / KRAS |
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| Research Abstract |
Our preliminary study revealed that FXYD3 expression was downregulated in oncogenic KRAS-transduced airway epithelial cells. This result interested us to investigate the role of FXYD3 in carcinogenesis of the lung. FXYD3 mRNA and protein levels were lower in most of the lung cancer cell lines than in either the non-cancerous lung tissue or airway epithelial cells. Its protein levels were lower in a considerable proportion of primary lung cancers than in non-tumoral airway epithelia. The levels reduced in parallel with the dedifferentiation process. Also, a somatic point mutation, g55c (D19H), was found in one cell line. Forced expression of the wild-type FXYD3, but not the mutant, restored the well-demarcated distribution of cortical actin in cancer cells that had lost FXYD3 expression, suggesting FXYD3 to play roles in the maintenance of cytoskeletal integrity. No association between its expression and the promoter's methylation status was observed. Inactivation of FXYD3 through a gene mutation or unknown mechanism could be one causes of the atypical shapes of cancer cells and play a potential role in the progression of lung cancer.
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