奧地利研究者最近發(fā)現(xiàn)了一種特殊的酶在惡性腫瘤形成中的作用機理,。這一發(fā)現(xiàn)可能有助于癌癥的早發(fā)現(xiàn),、早治療。
維也納醫(yī)科大學(xué)等機構(gòu)的研究人員在新一期《歐洲分子生物學(xué)組織通訊》上報告說，hdac（組蛋白去乙酰化酶）是一組可以影響細胞活動的酶,。此前有研究者推測，這組酶中的hdac1酶可能在腫瘤的形成過程中起到了重要作用。
奧地利研究人員以畸胎瘤為模型進行了研究,?；チ銎鹪从谏臣毎喟l(fā)現(xiàn)于卵巢中,?；チ鲭m然多為良性,，但隨著年齡的增長,，其惡性傾向也隨之上升。
此次研究顯示,，如果hdac1酶受到壓制,，良性畸胎瘤就會發(fā)生惡化。而此前有研究認為,，hdac1酶的過?？赡軐?dǎo)致瘤性組織生長失控。
參加此次研究的奧地利學(xué)者認為,，新的研究結(jié)果說明,，今后可以將hdac１酶視為一種瘤性組織可能發(fā)生惡變的“指標”，監(jiān)測腫瘤惡變跡象,。（生物谷Bioon.com）
生物谷推薦英文摘要：
The EMBO Journal doi:10.1038/emboj.2010.264
Crucial function of histone deacetylase 1 for differentiation of teratomas in mice and humans
Sabine Lagger1,5, Dominique Meunier1,5, Mario Mikula2,6, Reinhard Brunmeir1,7, Michaela Schlederer3, Matthias Artaker1, Oliver Pusch4, Gerda Egger3, Astrid Hagelkruys1, Wolfgang Mikulits2, Georg Weitzer1, Ernst W Muellner1, Martin Susani3, Lukas Kenner3,8 and Christian Seiser1,8
1 Department of Medical Biochemistry, Max F. Perutz Laboratories, Medical University of Vienna, Vienna Biocenter, Vienna, Austria
2 Institute for Cancer Research, Medical University of Vienna, Vienna, Austria
3 Clinical Institute for Pathology, Medical University of Vienna, Vienna, Austria
4 Center for Anatomy and Cell Biology, Medical University of Vienna, Vienna, Austria
Histone deacetylase (HDAC) inhibitors induce cell cycle arrest, differentiation or apoptosis in tumour cells and are, therefore, promising anti-cancer reagents. However, the specific HDAC isoforms that mediate these effects are not yet identified. To explore the role of HDAC1 in tumourigenesis and tumour proliferation, we established an experimental teratoma model using wild-type and HDAC1-deficient embryonic stem cells. HDAC1-deficient teratomas showed no significant difference in size compared with wild-type teratomas. Surprisingly, loss of HDAC1 was not only linked to increased apoptosis, but also to significantly enhanced proliferation. Epithelial structures showed reduced differentiation as monitored by Oct3/4 expression and changed E-cadherin localization and displayed up-regulated expression of SNAIL1, a regulator of epithelial cell plasticity. Increased levels of the transcriptional regulator SNAIL1 are crucial for enhanced proliferation and reduced differentiation of HDAC1-deficient teratoma. Importantly, the analysis of human teratomas revealed a similar link between loss of HDAC1 and enhanced tumour malignancy. These findings reveal a novel role for HDAC1 in the control of tumour proliferation and identify HDAC1 as potential marker for benign teratomas.
