2015年2月6日 訊 /生物谷BIOON/ --近日，來自愛因斯坦醫學院 ( Albert Einstein College of Medicine )等處的研究人員通過研究揭示了乳腺腫瘤中攜帶低水平前纖維蛋白1的細胞增加轉移及入侵其它組織能力的分子機理，相關研究發表於國際雜誌European Journal of Cell Biology上。
近些年來越來越多的研究都聚焦於開發抵禦癌症擴散的新型療法，然而目前並沒有開發出可以阻斷或抑制腫瘤從原發性位點擴散的有效療法；研究者José Javier Bravo-Cordero說道，文章中我們揭示了前纖維蛋白1如何參與形成腫瘤擴散的決定結構；利用高解析度的顯微鏡技術，我們就可以對缺失前纖維蛋白1的腫瘤細胞的樹突狀偽足的動態變化進行研究，並且描述其主要功能。
乳腺癌患者機體中的前纖維蛋白1水平往往較低，其和機體癌細胞轉移的能力增加直接相關，研究者表示，讓我們不可思議的是缺失前纖維蛋白1的細胞會通過偽足介導表現出較強的侵襲力，研究者在文章中也揭示了偽足內部結構及肌動蛋白骨架在其功能中的重要作用，同時也發現前纖維蛋白1在該調節過程中扮演著重要角色。
如果破壞了支架，偽足的關鍵結構就不會形成，以相同的方式，如果研究者可以對支架進行高效裝配並且形成偽足的結構，就可以使得癌細胞恢復高度擴散的能力；隨後研究者又描述了一種特殊的分子路徑，其可以使得偽足在缺失前纖維蛋白1的細胞中更具有侵襲性。
Alejandra Valenzuela-Iglesias指出，在蛋白平衡的情況下偽足會很快成熟成為具有高效功能的結構，並且通過抑制前纖維蛋白1來快速降解細胞基質，從而使得癌細胞的轉移能力增加。最後研究者表示，本文研究為開發新型療法抑制癌症轉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."