| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Research Abstract |
Renal cell carcinoma (RCC) is known to express CXCR3. CXCR3 can be considered as one of the Cancer/Testis Antigens. The function of CXCR3 on RCC has not been clarified. The aims of this study were to reveal the function of CXCR3. Fifty-six clinical samples of clear cell RCC and corresponding normal renal tissue samples were used.
CXCR3 and its ligands were abundant in RCC samples compared with corresponding normal kidney samples. CXCL10 treatment induced 786-O cell migration and invasion. In clinical samples, the expressions of CXCR3 and CXCR3-A were significantly higher in metastatic RCC than in non-metastatic RCC. Finally, the expression of CXCR3-A and hypoxia-inducible factor 1 alpha were significantly correlated in the clinical samples. Regarding 786-O, treatment with cobalt chloride (CoCl2) up-regulated CXCR3 expression 4.5-fold. We showed the association of CXCR3 and RCC metastasis. The expression of CXCR3 may be regulated by hypoxia.
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