法國(guó)國(guó)家健康與醫(yī)學(xué)研究所的研究人員日前發(fā)現(xiàn),，有兩種基因在癌細(xì)胞的擴(kuò)散中發(fā)揮了重要作用,，這一發(fā)現(xiàn)將為尋找癌癥治療方法提供新的思路,。
該研究所的一個(gè)研究小組7月11日發(fā)表公報(bào)說(shuō),，人體含有名為T(mén)wist1和Twist2的兩種基因,，它們是胚胎發(fā)育的“主要調(diào)控因子”,，但在正常成年人體內(nèi)它們一般都選擇“沉默”。不過(guò)研究人員通過(guò)實(shí)驗(yàn)發(fā)現(xiàn),，在很多癌癥病例當(dāng)中,，這兩種基因又重新被激活，它們能夠增強(qiáng)癌細(xì)胞侵略性和活動(dòng)性,，使其越過(guò)免疫系統(tǒng)的“防線”,，向其他器官擴(kuò)散。
研究小組的負(fù)責(zé)人阿蘭·皮敘認(rèn)為,，這一發(fā)現(xiàn)將有助于盡早發(fā)現(xiàn)惡性腫瘤以及研究癌癥的早期療法,，該研究成果已刊登在最新一期美國(guó)《癌細(xì)胞》（Cancer Cell）雜志上。（生物谷Bioon.com）
生物谷推薦原始出處：
Cancer Cell,，Vol 14, 79-89, 08 July 2008,，Stéphane Ansieau, Alain Puisieux
Induction of EMT by Twist Proteins as a Collateral Effect of Tumor-Promoting Inactivation of Premature Senescence
Stéphane Ansieau,1 Jeremy Bastid,1,2,6 Agnès Doreau,1,6 Anne-Pierre Morel,3,6 Benjamin P. Bouchet,1,2 Clémence Thomas,1,2 Frédérique Fauvet,3 Isabelle Puisieux,1 Claudio Doglioni,4 Sara Piccinin,5 Roberta Maestro,5 Thibault Voeltzel,1 Abdelkader Selmi,1,2 Sandrine Valsesia-Wittmann,1 Claude Caron de Fromentel,1 and Alain Puisieux1,2,3,
1 Inserm, U590, Lyon, F-69008, France
2 Université de Lyon, Lyon 1, Institut des Sciences Pharmaceutiques et Biologiques, Lyon, F-69008, France
3 Centre Léon Bérard, FNCLCC, Laboratoire de Recherche Translationnelle, Lyon, F-69008, France
4 Belluno City Hospital, Belluno, I-32100, Italy
5 CRO IRCCS, Aviano National Cancer Institute, Aviano, I-33081, Italy
Summary
Twist1 and Twist2 are major regulators of embryogenesis. Twist1 has been shown to favor the metastatic dissemination of cancer cells through its ability to induce an epithelial-mesenchymal transition (EMT). Here, we show that a large fraction of human cancers overexpress Twist1 and/or Twist2. Both proteins override oncogene-induced premature senescence by abrogating key regulators of the p53- and Rb-dependent pathways. Twist1 and Twist2 cooperate with Ras to transform mouse embryonic fibroblasts. Interestingly, in epithelial cells, the oncogenic cooperation between Twist proteins and activated mitogenic oncoproteins, such as Ras or ErbB2, leads to complete EMT. These findings suggest an unanticipated direct link between early escape from failsafe programs and the acquisition of invasive features by cancer cells.
