生物谷報(bào)道：美國研究人員最近發(fā)現(xiàn),，有些癌細(xì)胞可以釋放一種叫“骨橋蛋白”（osteopontin）的蛋白質(zhì),，這種蛋白質(zhì)會“喚醒”體內(nèi)休眠的癌細(xì)胞,。這一發(fā)現(xiàn)有助于醫(yī)生了解并預(yù)防癌細(xì)胞在體內(nèi)的擴(kuò)散。相關(guān)論文于6月13日發(fā)表在Cell上面,。
研究人員給實(shí)驗(yàn)鼠同時(shí)移植了兩種癌細(xì)胞：一種是被稱為“煽動者”（instigator）的腫瘤細(xì)胞,，是科學(xué)家在實(shí)驗(yàn)室用可快速生長的乳腺癌細(xì)胞培養(yǎng)成的，另一種是生長緩慢只是偶然發(fā)生轉(zhuǎn)移的俗稱“回應(yīng)者”的癌細(xì)胞,，這種癌細(xì)胞多數(shù)時(shí)間處于休眠狀態(tài),。
研究人員發(fā)現(xiàn)，“煽動者”腫瘤細(xì)胞的存在加速“回應(yīng)者”（responder）癌細(xì)胞繁殖,，使轉(zhuǎn)移的癌細(xì)胞增加９倍,。他們用從癌癥患者體內(nèi)采集的結(jié)腸癌細(xì)胞作為“回應(yīng)者”細(xì)胞重復(fù)實(shí)驗(yàn)，獲得了相似的結(jié)果,。
隨后的分析顯示,，“骨橋蛋白”是這種“煽動者”腫瘤細(xì)胞發(fā)揮作用的關(guān)鍵所在。研究人員于是阻止癌細(xì)胞中“骨橋蛋白”的生產(chǎn),，結(jié)果“煽動者”腫瘤細(xì)胞繼續(xù)生長繁殖,，卻不再刺激“回應(yīng)者”細(xì)胞。研究人員由此認(rèn)為,，這種蛋白質(zhì)會“喚醒”體內(nèi)休眠的癌細(xì)胞,，幫助它們占領(lǐng)新組織。
在此前的研究中,，研究人員一直將“骨橋蛋白”用作一種監(jiān)控癌瘤生長的生物標(biāo)記物,，并發(fā)現(xiàn)這種蛋白質(zhì)與包括乳腺癌和前列腺癌在內(nèi)的多種癌癥有直接關(guān)系。
目前,，研究人員正在研發(fā)能阻止這種蛋白質(zhì)發(fā)揮作用的藥物,，以用來對抗癌癥。（生物谷www.bioon.com）
生物谷推薦原始出處：
Cell, Vol 133, 994-1005, 13 June 2008
Systemic Endocrine Instigation of Indolent Tumor Growth Requires Osteopontin
Sandra S. McAllister,1 Ann M. Gifford,1,9 Ashley L. Greiner,1,2,9 Stephen P. Kelleher,1,3 Matthew P. Saelzler,1,4 Tan A. Ince,1,5 Ferenc Reinhardt,1 Lyndsay N. Harris,6 Bonnie L. Hylander,7 Elizabeth A. Repasky,7 and Robert A. Weinberg1,4,8,
1 Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA
2 The Department of Biology, Boston University, Boston, MA 02215, USA
3 Department of Biology, Williams College, Williamstown, MA 01267, USA
4 Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
5 Department of Pathology, Division of Women's and Perinatal Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA
6 Department of Medical Oncology, Yale University Medical Center, New Haven, CT 06510, USA
7 Department of Immunology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
8 MIT Ludwig Center for Molecular Oncology, Cambridge, MA 02142, USA
Summary
The effects of primary tumors on the host systemic environment and resulting contributions of the host to tumor growth are poorly understood. Here, we find that human breast carcinomas instigate the growth of otherwise-indolent tumor cells, micrometastases, and human tumor surgical specimens located at distant anatomical sites. This systemic instigation is accompanied by incorporation of bone-marrow cells (BMCs) into the stroma of the distant, once-indolent tumors. We find that BMCs of hosts bearing instigating tumors are functionally activated prior to their mobilization; hence, when coinjected with indolent cells, these activated BMCs mimic the systemic effects imparted by instigating tumors. Secretion of osteopontin by instigating tumors is necessary for BMC activation and the subsequent outgrowth of the distant otherwise-indolent tumors. These results reveal that outgrowth of indolent tumors can be governed on a systemic level by endocrine factors released by certain instigating tumors, and hold important experimental and therapeutic implications.
