1月5日，國際著名雜志Nature在線刊登了瑞士和中國科學(xué)家的最新研究成果“Interactions between cancer stem cells and their niche govern metastatic colonization,。”，文章中,，作者揭示了癌癥干細(xì)胞是如何構(gòu)建自己小環(huán)境的。
用一個(gè)小鼠乳腺腫瘤模型（在該模型中,，腫瘤細(xì)胞自然地向肺部轉(zhuǎn)移）所做實(shí)驗(yàn)表明,，轉(zhuǎn)移的腫瘤細(xì)胞要能“定殖”，首先需要少量有滲透力的癌癥干細(xì)胞的存在,。這些細(xì)胞誘導(dǎo)細(xì)胞外蛋白“骨膜蛋白”（該蛋白通過增強(qiáng)腫瘤細(xì)胞中的Wnt信號(hào)作用支持在所形成的小環(huán)境中轉(zhuǎn)移酶的生長）的表達(dá),。“骨膜蛋白”功能的阻斷阻止轉(zhuǎn)移的進(jìn)行，說明在轉(zhuǎn)移的早期階段,、當(dāng)腫瘤細(xì)胞很可能對小環(huán)境中的信號(hào)有特別依賴性時(shí),，以轉(zhuǎn)移小環(huán)境為目標(biāo)進(jìn)行治療可能具有治療潛力。（生物谷Bioon.com）
doi:10.1038/nature10694
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Interactions between cancer stem cells and their niche govern metastatic colonization
Ilaria Malanchi, Albert Santamaria-Martínez, Evelyn Susanto, Hong Peng, Hans-Anton Lehr, Jean-Francois Delaloye & Joerg Huelsken
Metastatic growth in distant organs is the major cause of cancer mortality. The development of metastasis is a multistage process with several rate-limiting steps1. Although dissemination of tumour cells seems to be an early and frequent event2, the successful initiation of metastatic growth, a process termed ‘metastatic colonization’, is inefficient for many cancer types and is accomplished only by a minority of cancer cells that reach distant sites3, 4. Prevalent target sites are characteristic of many tumour entities5, suggesting that inadequate support by distant tissues contributes to the inefficiency of the metastatic process. Here we show that a small population of cancer stem cells is critical for metastatic colonization, that is, the initial expansion of cancer cells at the secondary site, and that stromal niche signals are crucial to this expansion process. We find that periostin (POSTN), a component of the extracellular matrix, is expressed by fibroblasts in the normal tissue and in the stroma of the primary tumour. Infiltrating tumour cells need to induce stromal POSTN expression in the secondary target organ (in this case lung) to initiate colonization. POSTN is required to allow cancer stem cell maintenance, and blocking its function prevents metastasis. POSTN recruits Wnt ligands and thereby increases Wnt signalling in cancer stem cells. We suggest that the education of stromal cells by infiltrating tumour cells is an important step in metastatic colonization and that preventing de novo niche formation may be a novel strategy for the treatment of metastatic disease.
