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EJCB:揭示乳腺癌肿瘤抑制子前纤维蛋白1的关键角色

  1. 乳腺癌
  2. 前纤维蛋白
  3. 肿瘤抑制子
  4. 角色

来源:生物谷 2015-02-06 10:29

近日,来自爱因斯坦医学院 ( Albert Einstein College of Medicine )等处的研究人员通过研究揭示了乳腺肿瘤中携带低水平前纤维蛋白1的细胞增加转移及入侵其它组织能力的分子机理,相关研究发表于国际杂志European Journal of Cell Biology上。

2015年2月6日 讯 /生物谷BIOON/ --近日,来自爱因斯坦医学院 ( Albert Einstein College of Medicine )等处的研究人员通过研究揭示了乳腺肿瘤中携带低水平前纤维蛋白1的细胞增加转移及入侵其它组织能力的分子机理,相关研究发表于国际杂志European Journal of Cell Biology上。

近些年来越来越多的研究都聚焦于开发抵御癌症扩散的新型疗法,然而目前并没有开发出可以阻断或抑制肿瘤从原发性位点扩散的有效疗法;研究者José Javier Bravo-Cordero说道,文章中我们揭示了前纤维蛋白1如何参与形成肿瘤扩散的决定结构;利用高分辨率的显微镜技术,我们就可以对缺失前纤维蛋白1的肿瘤细胞的树突状伪足的动态变化进行研究,并且描述其主要功能。

乳腺癌患者机体中的前纤维蛋白1水平往往较低,其和机体癌细胞转移的能力增加直接相关,研究者表示,让我们不可思议的是缺失前纤维蛋白1的细胞会通过伪足介导表现出较强的侵袭力,研究者在文章中也揭示了伪足内部结构及肌动蛋白骨架在其功能中的重要作用,同时也发现前纤维蛋白1在该调节过程中扮演着重要角色。

如果破坏了支架,伪足的关键结构就不会形成,以相同的方式,如果研究者可以对支架进行高效装配并且形成伪足的结构,就可以使得癌细胞恢复高度扩散的能力;随后研究者又描述了一种特殊的分子路径,其可以使得伪足在缺失前纤维蛋白1的细胞中更具有侵袭性。

Alejandra Valenzuela-Iglesias指出,在蛋白平衡的情况下伪足会很快成熟成为具有高效功能的结构,并且通过抑制前纤维蛋白1来快速降解细胞基质,从而使得癌细胞的转移能力增加。最后研究者表示,本文研究为开发新型疗法抑制癌症转移提供了新的思路和希望。(生物谷Bioon.com)

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In recent years, medical professionals have been greatly interested in the development of new treatments to combat the spread of cancer, which is the largest cause of death in patients with this illness.
However, effective treatments have still not been developed to stop or prevent tumour cells spreading from their primary tumour, a critical step in the cancer reaching different organs during metastasis.
Now, a new study published in the 'European Journal of Cell Biology' and led by José Javier Bravo-Cordero, a Spanish researcher working in the Albert Einstein College of Medicine in New York (USA), reveals how the profilin 1 protein intervenes in the formation of determining structures for the tumour invasion.
"To obtain this level of effectiveness the tumour cells form a subcellular structure called invadopodia (from the Latin invado, invade, and podio, feet; invasive feet) and they use it to spread towards other parts of the organism," explains Bravo-Cordero.
Using high resolution microscope techniques, the authors have been able to study the dynamics of the invadopodia in tumour cells which lack profilin 1, and describe their role and the route they regulate.
Therefore patients with breast cancer tumours show reduced levels of the protein profilin 1, which is related to an increase in the capacity of the human breast tumours to metastasise other organs.
"Surprisingly, the cells which lack profilin 1 show extremely invasive activity mediated by the invadopodia, compared to control cells. It is as if we had taken the brake off and lost control of the vehicle," describes the Spanish scientist.
What is more, adds Bravo-Cordero, "in the absence of profilin 1 the invadopodia are more aggressive when it comes to degrading the extracellular matrix and are highly invasive structures, which explains the high metastatic potential of these cells."

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