大部分因癌癥而死亡的病例都是由于癌細(xì)胞擴(kuò)散到了肝臟或大腦等重要器官所導(dǎo)致,。
人體癌細(xì)胞資料圖
日前,，瑞士洛桑癌癥研究中心的科學(xué)家在PLos ONE雜志上發(fā)表論文"Identification of Prognostic Molecular Features in the Reactive Stroma of Human Breast and Prostate Cancer"稱發(fā)現(xiàn)了一種促進(jìn)腫瘤擴(kuò)散和轉(zhuǎn)移的“主力”蛋白質(zhì)——成骨細(xì)胞特異因子-2（Periostin）。研究人員實(shí)驗(yàn)證明,，控制這種蛋白質(zhì)的數(shù)量能夠有效抑制惡性腫瘤（癌細(xì)胞）的活躍程度。因此,，這一發(fā)現(xiàn)將有望給癌癥治療開辟一條全新的途徑,。
成骨細(xì)胞特異因子-2是一種細(xì)胞外基質(zhì)蛋白，一般存在于細(xì)胞之間的結(jié)締組織縫隙中,，對(duì)于胎兒骨骼的形成有重要作用,。研究小組負(fù)責(zé)人約爾格·許爾斯曼博士介紹說，研究人員在模擬腫瘤存活環(huán)境時(shí)發(fā)現(xiàn)了成骨細(xì)胞特異因子-2的上述作用,。
“我的同事們模擬了幾種適宜腫瘤存活,、并利于腫瘤擴(kuò)散形成癌細(xì)胞的環(huán)境，發(fā)現(xiàn)這種特別的蛋白質(zhì)對(duì)于惡性腫瘤的擴(kuò)散起著非常重要的作用,。”約爾格博士說,，“如果沒有這種蛋白質(zhì)的‘搬運(yùn)功能’，癌細(xì)胞就不能順利擴(kuò)散,，并會(huì)一直保持休眠狀態(tài),。也就是說，如果我們能夠控制這種蛋白質(zhì)的活躍程度,，就有望抑制癌細(xì)胞的進(jìn)一步擴(kuò)散和惡化,。”
科學(xué)家們已經(jīng)開始根據(jù)這一發(fā)現(xiàn)，研制能夠附著在這種蛋白質(zhì)外壁并導(dǎo)致其功能失調(diào)的抗體,，并希望這種抗體能夠幫助人類抵抗癌癥的侵害,。
“動(dòng)物實(shí)驗(yàn)證明我們的治療方法是行得通的，且不會(huì)產(chǎn)生太多的副作用,。雖然,，這并不代表這種抗體對(duì)人體同樣有效，而且我們也不確定能夠找到對(duì)人體有效的類似抗體,，但我們正在努力,。”約爾格博士說。
目前，大部分因癌癥而死亡的病例都是由于癌細(xì)胞擴(kuò)散到了肝臟或大腦等重要器官所導(dǎo)致的,。因此,，如果科學(xué)家能夠成功研制出抑制該種蛋白的人體抗體，對(duì)于癌癥治療來說將具有歷史性的意義,。（生物谷bioon.com）
相關(guān)新聞：
Oncogene：促使癌細(xì)胞擴(kuò)散的“幫兇”基因
科學(xué)家發(fā)現(xiàn)身體如何對(duì)抗癌細(xì)胞擴(kuò)散
PNAS：特定復(fù)合糖類可抑制癌細(xì)胞擴(kuò)散
JCB：miR22使細(xì)胞老化從而抑制癌細(xì)胞增殖和轉(zhuǎn)移
doi:10.1371/journal.pone.0018640
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PMID:
Identification of Prognostic Molecular Features in the Reactive Stroma of Human Breast and Prostate Cancer
Anne Planche1#, Marina Bacac1#, Paolo Provero2, Carlo Fusco1, Mauro Delorenzi3, Jean-Christophe Stehle1, Ivan Stamenkovic1*
Primary tumor growth induces host tissue responses that are believed to support and promote tumor progression. Identification of the molecular characteristics of the tumor microenvironment and elucidation of its crosstalk with tumor cells may therefore be crucial for improving our understanding of the processes implicated in cancer progression, identifying potential therapeutic targets, and uncovering stromal gene expression signatures that may predict clinical outcome. A key issue to resolve, therefore, is whether the stromal response to tumor growth is largely a generic phenomenon, irrespective of the tumor type or whether the response reflects tumor-specific properties. To address similarity or distinction of stromal gene expression changes during cancer progression, oligonucleotide-based Affymetrix microarray technology was used to compare the transcriptomes of laser-microdissected stromal cells derived from invasive human breast and prostate carcinoma. Invasive breast and prostate cancer-associated stroma was observed to display distinct transcriptomes, with a limited number of shared genes. Interestingly, both breast and prostate tumor-specific dysregulated stromal genes were observed to cluster breast and prostate cancer patients, respectively, into two distinct groups with statistically different clinical outcomes. By contrast, a gene signature that was common to the reactive stroma of both tumor types did not have survival predictive value. Univariate Cox analysis identified genes whose expression level was most strongly associated with patient survival. Taken together, these observations suggest that the tumor microenvironment displays distinct features according to the tumor type that provides survival-predictive value.
