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肺部是乳腺癌转移的首选器官

时间:2014年04月29日 信息来源:互联网 点击:

Lung-Derived Factors Mediate Breast Cancer Cell Migration through CD44 Receptor-Ligand Interactions in a Novel Ex Vivo System for Analysis of Organ-Specific Soluble Proteins   

     近日,国际闻名的学术期刊《肿瘤》杂志宣布关于乳腺癌转移的研究论文,论文称乳腺癌是头号癌症,是癌症女性患者死亡的重要缘故原由。假如及早发现,传统的化疗和放疗有较高的成功率,但一旦疾病蔓延,转移到身体其他部位,很多传统治疗会失败。近日,一项新的研究揭示了为什么乳腺癌每每蔓延或转移至肺部。肺是乳腺癌转移的最常见而致命的器官之一,对患者生命和生存质量有明显影响。研究小组早期注解,乳腺癌细胞的特定类型--乳腺癌干细胞(CSC)负责动物模型中的肺转移。研究人员开发了一种创新的前体(生物体外模型体系)模型体系,模仿不同器官环境。他们观察到乳腺肿瘤干细胞有向肺部迁移,并在肺部赓续增加的特定倾向,他们发现乳腺肿瘤干细胞与肺源性蛋白质之间的特异性相互作用可能被靶向打乱,以削减乳腺癌的肺转移举动。在转移过程中,有一个叫做种子和泥土假说理论。类似蒲公英种子,种子吹向所有的地方,但他们不肯定到处都生长,他们只在适宜的泥土中生长。在转移的情况下,肿瘤细胞(“种子”)有一些决定他们自身侵略性和转移能力的内在因素,而器官(“泥土”)被认为提供肿瘤细胞生长特定紧张因素,帮助支撑他们的生存,使其成长为转移性肿瘤。许多研究已经完成对癌细胞的研究,由于它们很容易研究,但对于“泥土”因素研究还不是许多。新研究已经发现产生于肺的一些特定的蛋白质,好像与癌症干细胞的相互作用,使肺部成为癌细胞生长的一个适宜器官,当然乳房最近的器官是肺,近距离转移也是可能。

        Breast cancer preferentially metastasizes to lung, lymph node, liver, bone, and brain. However, it is unclear whether properties of cancer cells, properties of organmicroenvironments, or a combination of both is responsible for this observed organ tropism. We hypothesized that breast cancer cells exhibit distinctive migration/growth patterns in organ microenvironments that mirror common clinical sites of breast cancer metastasis and that receptor-ligand interactions between breast cancer cells and soluble organ-derived factors mediate this behavior. Using an ex vivo model system composed of organ-conditionedmedia (CM), human breast cancer cells (MDA-MB-231,MDA-MB-468, SUM149, and SUM159) displayed cell line—specific and organ-specific patterns of migration/proliferation that corresponded to their in vivo metastatic behavior. Notably, exposure to lung-CM increased migration of all cell lines and increased proliferation in two of four lines (P < .05). Several cluster of differentiation (CD) 44 ligands including osteopontin (OPN) and L-selectin (SELL) were identified in lung-CM by protein arrays. Immunodepletion of SELL decreased migration of MDA-MB-231 cells, whereas depletion of OPN decreased both migration and proliferation. Pretreatment of cells with a CD44-blocking antibody abrogated migration effects (P < .05). “Stemlike” breast cancer cells with high aldehyde dehydrogenase and CD44 (ALDHhiCD44+) responded in a distinct chemotacticmanner toward organ-CM, preferentially migrating toward lung-CM through CD44 receptor-ligand interactions (P < .05). In contrast, organ-specific changes in migration were not observed for ALDHlowCD44- cells. Our data suggest that interactions between CD44+ breast cancer cells and soluble factors present in the lung microenvironment may play an important role in determining organotropic metastatic behavior.

 

 


 


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