奥地利研究者最近发现了一种特殊的酶在恶性肿瘤形成中的作用机理。这一发现可能有助于癌症的早发现、早治疗。
维也纳医科大学等机构的研究人员在新一期《欧洲分子生物学组织通讯》上报告说，hdac（组蛋白去乙酰化酶）是一组可以影响细胞活动的酶。此前有研究者推测，这组酶中的hdac1酶可能在肿瘤的形成过程中起到了重要作用。
奥地利研究人员以畸胎瘤为模型进行了研究。畸胎瘤起源于生殖细胞，多发现于卵巢中。畸胎瘤虽然多为良性，但随着年龄的增长，其恶性倾向也随之上升。
此次研究显示，如果hdac1酶受到压制，良性畸胎瘤就会发生恶化。而此前有研究认为，hdac1酶的过剩可能导致瘤性组织生长失控。
参加此次研究的奥地利学者认为，新的研究结果说明，今后可以将hdac１酶视为一种瘤性组织可能发生恶变的“指标”，监测肿瘤恶变迹象。（生物谷Bioon.com）
生物谷推荐英文摘要：
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.
