本期Nature Communications在線介紹了用來模擬癌細胞與非癌細胞之間界面的一個新的、更精確的方法。這一方法也許能夠提升我們對腫瘤發(fā)展以及治療干預(yù)措施療效的認識。

癌癥發(fā)展已被與基因表達的復(fù)雜變化聯(lián)系了起來，在其中細胞的精確物理位置似乎也起一定作用——靠近癌細胞與正常細胞之間界面的細胞會與那些相距較遠的細胞具有不同的基因表達特征。

Biju Parekkadan及同事建立了一個新系統(tǒng)，它使其能夠?qū)┘毎头前┘毎M織到截然不同的空間腔室中，然后采用基于顯微鏡的激光捕捉方法來將單個細胞解析出來，以進行分子分析。

采用他們的新方法，本文作者得以能夠顯示一種名為“reversine”的抗癌藥物何以在那些物理上靠近癌細胞和正常細胞之間界面的細胞中有最強效應(yīng)，該發(fā)現(xiàn)隨后在用小鼠所做的試驗中得到證實。這一模型有可能被用來揭示以相似方式發(fā)揮作用的其他藥物的療效以及對現(xiàn)有抗癌藥物的治療方案進行優(yōu)化。

原文標題：Resolving cancer–stroma interfacial signalling and interventions with micropatterned tumour–stromal assays

原文摘要：Tumour–stromal interactions are a determining factor in cancer progression. In vivo, the interaction interface is associated with spatially resolved distributions of cancer and stromal phenotypes. Here, we establish a micropatterned tumour–stromal assay (μTSA) with laser capture microdissection to control the location of co-cultured cells and analyse bulk and interfacial tumour–stromal signalling in driving cancer progression. μTSA reveals a spatial distribution of phenotypes in concordance with human ?oestrogen receptor-positive (?ER+) breast cancer samples, and heterogeneous drug activity relative to the tumour–stroma interface. Specifically, an unknown mechanism of ?reversine is shown in targeting tumour–stromal interfacial interactions using ?ER+ MCF-7 breast cancer and bone marrow-derived stromal cells. Reversine suppresses MCF-7 tumour growth and bone metastasis in vivo by reducing tumour stromalization including collagen deposition and recruitment of activated stromal cells. This study advocates μTSA as a platform for studying tumour microenvironmental interactions and cancer field effects with applications in drug discovery and development.

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