根据来自澳大利亚布里斯班的科学家的最新研究结果，雌性激素能打开和乳腺癌相关的基因。研究小组来自Queensland大学的Diamantina肿瘤、免疫和代谢医学研究所，他们相信这一发现将帮助解释乳腺癌和病人体内高浓度雌激素之间存在的关系。
Diamantina的癌症生物学负责人Tom Gonda教授表示：“我们的结果证明了雌性激素打开这一基因的能力对于乳腺癌细胞的生长非常重要。”
科学家们提到的基因被称为MYB，它在大约70％的乳腺癌患者体内都存在，并且这也是数十个能促进肿瘤生长的致癌基因之一。
Gonda教授说：“对于乳腺癌而言，真正重要的是雌性激素打开MYB基因的能力，而不是基因自身发生的变异。”他还表示小组下一步的研究计划是将这些得到的结果在实验室的老鼠身上进行测试，之前的结果是从实验室分离的癌细胞上得到的，而老鼠无疑是更好的研究模型。
Gonda教授认为：“我们正在尝试直接证明MYB基因能在健康的乳房组织中诱导出癌变。”Gonda教授和他Queensland大学的同事和来自墨尔本、阿德莱德以及美国的科学家进行了合作，并将他们的发现发表在本周出版的著名学术刊物《Proceedings of the National Academy of Sciences of the USA》上。Gonda表示，能阻止MYB活动的药物在将来或许可以用来治疗乳腺癌，但是他同时警告这还需要很长时间的艰苦研究才能实现。
（教育部科技发展中心）
原文链接：http://www.physorg.com/news107176889.html
原始出处:
Published online before print August 9, 2007, 10.1073/pnas.0700104104
PNAS | August 21, 2007 | vol. 104 | no. 34 | 13762-13767
Mechanism of and requirement for estrogen-regulated MYB expression in estrogen-receptor-positive breast cancer cells
Yvette Drabsch*, Honor Hugo,, Rui Zhang*,, Dennis H. Dowhan*, Yu Rebecca Miao,, Alan M. Gewirtz¶, Simon C. Barry||, Robert G. Ramsay,, and Thomas J. Gonda*,**
*University of Queensland Diamantina Institute for Cancer, Immunology, and Metabolic Medicine, Brisbane, Queensland 4102, Australia; Peter MacCallum Cancer Centre, Melbourne, Victoria 3002, Australia; Pathology Department, University of Melbourne, Victoria 3050, Australia; ¶Division of Hematology/Oncology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104; and ||Department of Paediatrics, University of Adelaide, South Australia 5006, Australia
Edited by Suzanne Cory, The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia, and approved June 29, 2007 (received for review January 7, 2007)
MYB (the human ortholog of c-myb) is expressed in a high proportion of human breast tumors, and that expression correlates strongly with estrogen receptor (ER) positivity. This may reflect the fact that MYB is a target of estrogen/ER signaling. Because in many cases MYB expression appears to be regulated by transcriptional attenuation or pausing in the first intron, we first investigated whether this mechanism was involved in estrogen/ER modulation of MYB. We found that this was the case and that estrogen acted directly to relieve attenuation due to sequences within the first intron, specifically, a region potentially capable of forming a stem–loop structure in the transcript and an adjacent poly(dT) tract. Secondly, given the involvement of MYB in hematopoietic and colon tumors, we also asked whether MYB was required for the proliferation of breast cancer cells. We found that proliferation of ER+ but not ER– breast cancer cell lines was inhibited when MYB expression was suppressed by using either antisense oligonucleotides or RNA interference. Our results show that MYB is an effector of estrogen/ER signaling and provide demonstration of a functional role of MYB in breast cancer.
antisense | cell cycle | proliferation | short hairpin RNA | transcriptional attenuation
