A new strategy of molecular targeting therapy for ovarian clear cell adenocinoma using transforming growth factor-betal(TGFβ1)
A new strategy of molecular targeting therapy for ovarian clear cell adenocinoma using transforming growth factor-betal(TGFβ1)
批准号:
18591850
负责人:
KOMIYAMA Shin-ichi
金额:
$2.49万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2006
资助国家:
日本
项目状态:
已结题
起止时间:
2006 至 2007
中文摘要
我们研究了转化生长因子-β1(转化生长因子-β1,β-1)分子靶向治疗卵巢透明细胞腺癌的基础研究。几种人卵巢透明细胞腺癌细胞(RMG-1、RMG-2和MO)在体外均表现出生长抑制、G1期停滞和侵袭抑制。RMG-1表达由TGFf31转录的p57mRNA和PAI-1mRNA,呈剂量依赖关系。另一方面,MIVIP2蛋白表达受到抑制。然后在SCID小鼠体内建立RMG-1异种移植模型,通过湿重和BrdU摄取量来评估肿瘤的生长。在荷瘤小鼠中,转化生长因子β1处理的肿瘤重量和对BrdU的摄取量都较低。此外,转化生长因子β1联合几种细胞毒药物(紫杉醇、SN-38和顺铂)在体外对RMG-1具有明显的生长抑制作用。
英文摘要
We studied a basic research for a new molecular targeting therapy for ovarian clear cell adenocarcinoma using transforming growth factor-beta 1 (TGFβ1). Several cell lines of human ovarian clear cell adenocarcinoma (RMG-1, RMG-2, and MO were demonstrated growth inhibition, G1 arrest, and invasion inhibition by TGFBI in vitro. RMG-1 expressed p57 mRNA and PAI-1 mRNA transcribed by TGFf31, dose-dependently. On the other hand, MIVIP2 protein expression was suppressed. Then xenograft models of RMG-1 were created in SCID mice, and tumor growth was assessed from the wet weight and the BrdU uptake. In tumor-bearing mice, the tumor weight and BrdU uptake were both lower when they were treated by TGFβ1. Furthermore, TGFβ1 combined several cytotoxic drugs (paclitaxel, SN-38, and CDDP) demonstrated growth inhibition additively for RMG-1 in vitro.
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DOI:
--
发表时间:
2006
期刊:
Acta cytologica 50
影响因子:
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DOI:
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发表时间:
2007
期刊:
影响因子:
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DOI:
--
发表时间:
2007
期刊:
影响因子:
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作者:
[Komiyama S, et. al.]
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DOI:
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发表时间:
2007
期刊:
影响因子:
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作者:
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DOI:
--
发表时间:
2007
期刊:
日本臨床 66
影响因子:
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作者:
[小宮山 慎一, 他]
通讯作者:
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