癌細胞的轉(zhuǎn)移是腫瘤的一種特殊本領(lǐng)，癌細胞能從原發(fā)部位沿著各種渠道到達身體的其他部位后繼續(xù)生長,，形成新的癌塊,，這種現(xiàn)象稱為癌轉(zhuǎn)移也叫癌擴散。要想治愈癌癥,，首先就要防止癌細胞的擴散,。來自紀念斯隆－凱特琳癌癥中心（Memorial Sloan Kettering Cancer Center）的研究人員獲得了腫瘤相關(guān)巨噬細胞在促進惡性腫瘤擴增方面的新機制,。這一研究成果公布在Genes & Development雜志上,。
天然免疫細胞，包括巨噬細胞在內(nèi),，都是腫瘤浸潤細胞環(huán)境中的一個重要組成部分,，即所謂的“腫瘤微環(huán)境”，腫瘤與其微環(huán)境之間存在動力學(xué)關(guān)聯(lián),，能通過一些分泌因子調(diào)控細胞的生長和癌癥的擴散,。
在這篇文章中，研究人員Johanna Joyce等人發(fā)現(xiàn)了這種腫瘤相關(guān)巨噬細胞（tumor-associated macrophages,，TAMs）是如何促進腫瘤生長和入侵的新機制,，他們發(fā)現(xiàn)巨噬細胞能浸入胰腺，乳腺和肺部癌細胞中,，高度表達蛋白酶cathepsin B和cathepsin S,，從而導(dǎo)致腫瘤的生長和侵入。
而且有趣的是,，研究人員還發(fā)現(xiàn)腫瘤本身還能促進cathepsin B和cathepsin S的活性增強,，這主要是通過interleukin(IL)-4的介導(dǎo)作用。
這項研究為靶向腫瘤微環(huán)境的癌癥治療提供了新證據(jù)和新工具,，靶向腫瘤微環(huán)境的癌癥治療也是目前擾亂癌癥擴散擴增的一種重要方法,。Joyce博士樂觀的認為這種方法能選擇性的靶向癌細胞通訊中的細胞，具有極大的治療前景,。（生物谷Bioon.com）
癌細胞轉(zhuǎn)移影響因素：
Science：癌癥轉(zhuǎn)移可能比預(yù)想的早
Nature：與乳腺癌腫瘤形成和轉(zhuǎn)移有關(guān)的兩種miRNA
Cell：特殊細胞因子促使乳腺腫瘤轉(zhuǎn)移
Nature Reviews Cancer：科學(xué)家提出癌癥轉(zhuǎn)移新解釋
PNAS：非編碼RNA可控制癌癥轉(zhuǎn)移
Cell Stem Cell：癌癥干細胞控制腫瘤轉(zhuǎn)移假說被證實
Cancer Research：苔蟲內(nèi)酯抗腫瘤轉(zhuǎn)移作用機理
Nature：科學(xué)家發(fā)現(xiàn)阻斷癌癥轉(zhuǎn)移的靶基因
PLoS ONE：巨噬細胞可幫助癌細胞轉(zhuǎn)移
生物谷推薦原始出處：
Genes & Development January 15, 2010, doi:10.1101/gad.1874010
IL-4 induces cathepsin protease activity in tumor-associated macrophages to promote cancer growth and invasion
Vasilena Gocheva1, Hao-Wei Wang1, Bedrick B. Gadea, Tanaya Shree, Karen E. Hunter, Alfred L. Garfall, Tara Berman and Johanna A. Joyce2
Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA
Innate immune cells can constitute a substantial proportion of the cells within the tumor microenvironment and have been associated with tumor malignancy in patients and animal models of cancer; however, the mechanisms by which they modulate cancer progression are incompletely understood. Here, we show that high levels of cathepsin protease activity are induced in the majority of macrophages in the microenvironment of pancreatic islet cancers, mammary tumors, and lung metastases during malignant progression. We further show that tumor-associated macrophage (TAM)-supplied cathepsins B and S are critical for promoting pancreatic tumor growth, angiogenesis, and invasion in vivo, and markedly enhance the invasiveness of cancer cells in culture. Finally, we demonstrate that interleukin-4 (IL-4) is responsible for inducing cathepsin activity in macrophages in vitro and in vivo. Together, these data establish IL-4 as an important regulator, and cathepsin proteases as critical mediators, of the cancer-promoting functions of TAMs.
