加拿大科學(xué)家近日研究發(fā)現(xiàn)，癌細(xì)胞能夠通過(guò)釋放囊泡與別的細(xì)胞進(jìn)行“通訊”,。這些囊泡含有致癌蛋白，當(dāng)融入到非惡性或輕度惡性細(xì)胞后,，它們能夠引發(fā)特定的機(jī)制,，促進(jìn)腫瘤生長(zhǎng)。這一發(fā)現(xiàn)將改變我們對(duì)癌組織活動(dòng)機(jī)制的認(rèn)識(shí),，并有可能導(dǎo)致大的臨床改革,。相關(guān)論文4月20日在線(xiàn)發(fā)表于《自然—細(xì)胞生物學(xué)》（Nature Cell Biology）上。
領(lǐng)導(dǎo)此次研究的是加拿大麥吉爾大學(xué)的Janusz Rak,。他和同事發(fā)現(xiàn),，腦腫瘤細(xì)胞膜上的一種表皮生長(zhǎng)因子受體III型突變體（EGFRvIII，一種致癌蛋白）能夠引發(fā)產(chǎn)生小的囊泡,，這些囊泡攜帶著數(shù)個(gè)EGFRvIII的變異副本,，研究人員將它們命名為“致癌組”（oncosomes）。令人非常吃驚的是,，這些囊泡并不會(huì)被限制在產(chǎn)生它們的細(xì)胞中,，它們也能夠轉(zhuǎn)移。
研究發(fā)現(xiàn),，這些轉(zhuǎn)移的致癌組會(huì)與其它健康或良性腫瘤細(xì)胞融合,。接著，EGFRvIII會(huì)融入到這些細(xì)胞的細(xì)胞膜中,，開(kāi)始刺激特定的代謝途徑以異常和惡性的方式活動(dòng),。雖然這可能是個(gè)短暫的現(xiàn)象，但是這種變化能夠通過(guò)快速增加細(xì)胞數(shù)量和刺激血管生長(zhǎng)（惡性腦腫瘤的特征）影響腫瘤的行為,。
Rak表示,，“這一研究證明了癌癥是一個(gè)多細(xì)胞的過(guò)程，其中廣泛地存在著細(xì)胞之間相互‘交談’的情況,。這與傳統(tǒng)的觀點(diǎn)——單個(gè)變異細(xì)胞不受控制地增殖以至形成腫瘤——背道而馳,。此次發(fā)現(xiàn)打開(kāi)了令人激動(dòng)的新研究途徑，我們同樣希望它能夠?yàn)榘┌Y患者帶來(lái)積極的效果,。”
在醫(yī)學(xué)實(shí)踐上,，癌癥患者血液中致癌組的出現(xiàn)可作為臨床標(biāo)記，這意味著醫(yī)生不必施行入侵性的外科手術(shù)或活組織檢查就可以篩選腫瘤的分子特征,。這無(wú)疑又朝著以人為本的個(gè)體化醫(yī)療邁進(jìn)了重要一步,。（科學(xué)網(wǎng) 梅進(jìn)/編譯）
生物谷推薦原始出處：
（Nature Cell Biology）,，doi:10.1038/ncb1725，Khalid Al-Nedawi,，Janusz Rak
Intercellular transfer of the oncogenic receptor EGFRvIII by microvesicles derived from tumour cells
Khalid Al-Nedawi1, Brian Meehan1, Johann Micallef3, Vladimir Lhotak2, Linda May2, Abhijit Guha3 & Janusz Rak1
Abstract
Aggressive human brain tumours (gliomas) often express a truncated and oncogenic form of the epidermal growth factor receptor, known as EGFRvIII. Within each tumour only a small percentage of glioma cells may actually express EGFRvIII; however, most of the cells exhibit a transformed phenotype1. Here we show that EGFRvIII can be 'shared' between glioma cells by intercellular transfer of membrane-derived microvesicles ('oncosomes'). EGFRvIII expression in indolent glioma cells stimulates formation of lipid-raft related microvesicles containing EGFRvIII. Microvesicles containing this receptor are then released to cellular surroundings and blood of tumour-bearing mice, and can merge with the plasma membranes of cancer cells lacking EGFRvIII. This event leads to the transfer of oncogenic activity, including activation of transforming signalling pathways (MAPK and Akt), changes in expression of EGFRvIII-regulated genes (VEGF, Bcl-xL, p27), morphological transformation and increase in anchorage-independent growth capacity. Thus, membrane microvesicles of cancer cells can contribute to a horizontal propagation of oncogenes and their associated transforming phenotype among subsets of cancer cells.
