Novel treatment of non-small cell lung cancer with the inhibition of IL-26-induced tumor angiogenesis
| Project/Area Number |
17590775
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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 |
Respiratory organ internal medicine
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| Research Institution | TOHOKU UNIVERSITY |
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Principal Investigator |
NUMASAKI Muneo TOHOKU UNIVERSITY, Tohoku University Hospital, Research Associate (50344677)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Takashi TOHOKU UNIVERSITY, Faculty of Medicine, Professor (10261629)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | angiogenesis / cytokine / non-small cell lung cancer / 肺癌 |
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| Research Abstract |
In this study, we examined the biological action of IL-26 on human non-small cell lung cancer (NSCLC). While IL-26 had no direct effect on the in vitro growth rate of NSCLC, IL-26 selectively augmented the secretion of an array of angiogenic CXC chemokines including CXCL1, CXCL5, CXCL6 and CXCL8, but not angiostatic chemokines, by two different NSCLC lines. Transfection with IL-26 into NSCLC had no effect on the in vitro growth, whereas IL-26 transfectants grew more rapidly compared with controls when transplanted in SCID mice. This IL-26-elicited enhanced NSCLC growth was associated with increased tumor vascularity. Moreover, treatment with anti-mouse CXCR-2 neutralizing Ab significantly attenuated the growth of both Neo- and IL-26-transfected NSCLC tumors in SCID mice. These results demonstrate that IL-26 increases the net angiogenic activity and in vivo growth of NSCLC via promoting CXCR-2-dependent angiogenesis and suggest that targeting CXCR-2 signaling may be a novel promising strategy to treat patients with NSCLC.
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Report
(3 results)
Research Products
(7 results)
