CIZ/NMP4 is expressed in B16 melanoma and forms a positive feedback loop with RANKL to promote migration of the melanoma cells

SakumaT.; NakamotoT.; HemmiH.KitazawaS.KitazawaR.NotomiT.HayataT.EzuraY.AmagasaT.NodaM.

首页> 外文期刊>Journal of Cellular Physiology >CIZ/NMP4 is expressed in B16 melanoma and forms a positive feedback loop with RANKL to promote migration of the melanoma cells

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CIZ/NMP4 is expressed in B16 melanoma and forms a positive feedback loop with RANKL to promote migration of the melanoma cells

机译：CIZ / NMP4表示在黑色素瘤B16转椅和形式和RANKL促进积极的反馈回路黑色素瘤细胞的迁移

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Tumor metastasis to bone is a serious pathological situation that causes severe pain, and deterioration in locomoter function. However, the mechanisms underlying tumor metastasis is still incompletely understood. CIZ/NMP4 is a nucleocytoplasmic shuttling protein and its roles in tumor cells have not been known. We, therefore, hypothesized the role of CIZ/NMP4 in B16 melanoma cells that metastasize to bone. CIZ/NMP4 is expressed in B16 cells. The CIZ/NMP4 expression levels are correlated to the metastatic activity in divergent types of melanoma cells. Overexpression of CIZ/NMP4 increased B16 cell migration in Trans-well assay. Conversely, siRNA-based knockdown of CIZ/NMP4 suppressed migratory activity of these cells. As RANKL promotes metastasis of tumor cells in bone, we tested its effect on CIZ in melanoma cells. RANKL treatment enhanced CIZ/NMP4 expression. This increase of CIZ by RANKL promoted migration. Conversely, we identified CIZ/NMP4 binding site in the promoter of RANKL. Furthermore, luciferase assay indicated that CIZ/NMP4 overexpression enhanced RANKL promoter activities, revealing a positive feedback loop of CIZ/NMP4 and RANKL in melanoma. These observations indicate that CIZ/NMP4 is critical regulator of metastasis of melanoma cells.

机译：骨肿瘤转移是一个严重的病态引起剧烈疼痛的情况,移动功能的恶化。肿瘤转移机制仍在不完全理解。核质穿梭于蛋白质和其角色在肿瘤细胞没有。因此,假设CIZ / NMP4的角色B16转椅黑色素瘤细胞转移至骨。CIZ / NMP4 B16转椅细胞中表达。的表达水平相关在不同类型的转移性活动黑色素瘤细胞。增加B16转椅Trans-well测定细胞迁移。相反,siRNA-based CIZ / NMP4击倒抑制这些细胞的迁徙活动。RANKL促进转移的肿瘤细胞在骨,我们测试了它对CIZ在黑色素瘤细胞的影响。RANKL治疗增强CIZ / NMP4表达式。这增加的CIZ RANKL促进迁移。相反,我们发现CIZ / NMP4结合位点在RANKL的启动子。试验表明,CIZ / NMP4超表达增强RANKL子活动,揭示一个积极的反馈回路CIZ / NMP4和RANKL在黑素瘤。CIZ / NMP4监管机构的转移是至关重要的黑色素瘤细胞。

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《Journal of Cellular Physiology》 |2012年第7期|2807-2812|共6页
作者
SakumaT.; NakamotoT.; HemmiH.KitazawaS.KitazawaR.NotomiT.HayataT.EzuraY.AmagasaT.NodaM.;
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Molecular Pharmacology Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan;

Kobe University, Division of Molecular Pathology, Kobe, 650-0017, Japan;

Tokyo Medical and Dental University, Tokyo, JapanMolecular Pharmacology Medical Research Institute, Tokyo Medical and Dental University, TokyoEhime University, Graduate School of Medicine, Division of Molecular Pathology, Ehime, Japan;

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正文语种英语
中图分类细胞生物学;
关键词
bone structure; melanoma cell; MelanomaNeoplastic CellImmigrationNeoplasm MetastasisPositive feedbackNucleo cytoplasmic Transportosteoclast differentiation factormetastasisFeedback loopB16 Melanoma;

机译：骨骼结构;黑色素瘤细胞;MelanomaNeoplasticCellImmigrationNeoplasm MetastasisPositivefeedbackNucleo细胞质Transportosteoclast分化factormetastasisFeedback loopB16黑素瘤;

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CIZ/NMP4 is expressed in B16 melanoma and forms a positive feedback loop with RANKL to promote migration of the melanoma cells

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