| Project/Area Number |
18591756
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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 |
Urology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
OKA Natsuo The University of Tokushima, University Medical and Dental Hospital, Assistant professor (40335790)
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| Co-Investigator(Kenkyū-buntansha) |
KANAYAMA Hiro-omi The University of Tokushima, Institute of Health Biosciences, Graduate school, professor (10214446)
TAKAHASHI Masayuki The University of Tokushima, University Medical and Dental Hospital, lecturer (50325255)
FUKUMORI Tomoharu The University of Tokushima, Institute of Health Bioscience, Graduate school, lecturer (10314874)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥300,000)
Fiscal Year 2007: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2006: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | Galectin-3 / TRAIL / apoptosis / Akt / 浸潤 / 転移 / アポトーシス / ガレクチン-3 |
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| Research Abstract |
Galectin-3 is a member of the family of β-galactoside binding mammalian lectins that is expressed at elevated levels in a variety of neoplastic cell types and has been implicated in tumor invasion and metastatic process, and apoptosis, though there are still some conflicting data regarding a certain type of tumors. To date, in urological cancer field, few experimental and clinical evidences have been reported regarding galectin-3 and cancer invasion in terms of apoptosis. We studied the expression of galecin-3 in renal cell carcinoma cell lines and human renal cell carcinoma tissues by RT-PCR and western blot analysis, and investigated the clinical significance and the possibility as a tumor marker. The expression of galectin-3 was identified in every renal cell carcinoma cell line we employed and was significantly higher in human renal cell carcinoma tissues than normal kidney tissues (418.6±137.3 vs 66.7±13.5, p=0.019). Especially in the case with metastasis, the expression ratio was
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significantly high (p=0.035), which suggested that ratio could become prognostic factor of metastasis. Similarly, in metastasis cases, the expressions of the genes associated with angiogenesis or TRAIL-induced apoptosis were elevated in proportion to that of galectin-3.
We observed that RT4 cells had very low level of constitutively active Akt and were sensitive to TRAIL, while UM-UC-3 and T24 cells had higher level of constitutively active Alt and were resistant to TRAIL. The expression level of active Akt was higher in galectin-overexpressed cells than that in wild type cells, though total expression level of Akt were similar between these cells, implicating the relation of galectin-3 in TRAIL resistance. 50% Galectin-3 knocked down cells demonstrated the decrease of active Akt expression to the same extent as that down-regulated by PI3K inhibitors.
Considering application to clinical field in future, some biological modulation will be required to find the possibility of galectin-3 as apoptosis inducing factor in urological cancers. Less
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