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　　在全世界范圍內(nèi)，胃癌是惡性疾病中第二位常見的致死病因。然而，利物浦大學(xué)的新研究發(fā)現(xiàn)，通過恢復(fù)TGFβig-h3蛋白的功能，可能有助于未來胃癌治療新手段的開發(fā)。利物浦大學(xué)的科學(xué)家發(fā)現(xiàn)，在胃癌患者體內(nèi)，一種可以防止腫瘤細(xì)胞生長和播散的蛋白，其生成情況受到了損害。

　　該蛋白是由肌纖維母細(xì)胞釋放的，此類細(xì)胞部分構(gòu)成了癌細(xì)胞周邊的支持組織。肌纖維母細(xì)胞、血管及其他類型細(xì)胞，其質(zhì)量占整個(gè)瘤體質(zhì)量的70%-90%，是癌細(xì)胞賴以存活的周邊環(huán)境。

　　肌纖維母細(xì)胞是具有高度活動(dòng)性的細(xì)胞，它可以產(chǎn)生并釋放多種物質(zhì)，通過改變腫瘤的周邊環(huán)境，改變腫瘤的行為學(xué)，導(dǎo)致癌細(xì)胞生長和播散。利物浦大學(xué)的科學(xué)家發(fā)現(xiàn)，在晚期胃癌患者的腫瘤瘤體中，由肌纖維母細(xì)胞所釋放的、正常狀態(tài)下能夠抑制腫瘤生長和播散的蛋白，其生成量減少了。

　　“在正常狀態(tài)下，上述蛋白可以將癌細(xì)胞和其周邊環(huán)境中的多種蛋白固定在一起，使得癌細(xì)胞與其適宜生長的環(huán)境隔絕開來。這種蛋白可作為靶向治療的靶點(diǎn)，但在晚期癌癥患者中，該蛋白效應(yīng)減弱，以致腫瘤向身體其他部位轉(zhuǎn)移的風(fēng)險(xiǎn)增高了。”利物浦大學(xué)轉(zhuǎn)化醫(yī)學(xué)研究所的Andrea Varro教授解釋道，“我們希望，通過上述蛋白的功能恢復(fù)，在未來可以開發(fā)出新的治療手段，繼而有助于使罹患胃癌這種常見致死性疾病的患者達(dá)到長期康復(fù)。”

　　Release of TGFβig-h3 by gastric myofibroblasts slows tumor growth and is decreased with cancer progression.

　　Carcinogenesis 2012 Aug;33(8):1553-62 PMID:22610072

　　Holmberg C,Quante M,Steele I,Kumar JD,Balabanova S,Duval C,Czepan M,Rakonczay Z Jr,Tiszlavicz L,Nemeth I,Lazar G,Simonka Z,Jenkins R,Hegyi P,Wang TC,Dockray **,Varro A

　　Department of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.

　　Myofibroblasts; Stomach; Transforming Growth Factors

　　Tumor progression has been linked to changes in the stromal environment. Myofibroblasts are stromal cells that are often increased in tumors but their contribution to cancer progression is not well understood. Here, we show that the secretomes of myofibroblasts derived from gastric cancers [cancer-associated myofibroblasts (CAMs)] differ in a functionally significant manner from those derived from adjacent tissue [adjacent tissue myofibroblasts (ATMs)]. CAMs showed increased rates of migration and proliferation compared with ATMs or normal tissue myofibroblasts (NTMs). Moreover, conditioned medium (CM) from CAMs significantly stimulated migration, invasion and proliferation of gastric cancer cells compared with CM from ATMs or NTMs. Proteomic analysis of myofibroblast secretomes revealed decreased abundance of the extracellular matrix (ECM) adaptor protein like transforming growth factor-β-induced gene-h3 (TGFβig-h3) in CAMs, which was correlated with lymph node involvement and shorter survival. TGFβig-h3 inhibited IGF-II-stimulated migration and proliferation of both cancer cells and myofibroblasts, and suppressed IGF-II activation of p42/44 MAPkinase; TGFβig-h3 knockdown increased IGF-II- and CM-stimulated migration. Furthermore, administration of TGFβig-h3 inhibited myofibroblast-stimulated growth of gastric cancer xenografts. We conclude that stromal cells exert inhibitory as well as stimulatory effects on tumor cells; TGFβig-h3 is a stromal inhibitory factor that is decreased with progression of gastric cancers.