根據(jù)來(lái)自澳大利亞布里斯班的科學(xué)家的最新研究結(jié)果,，雌性激素能打開(kāi)和乳腺癌相關(guān)的基因。研究小組來(lái)自Queensland大學(xué)的Diamantina腫瘤,、免疫和代謝醫(yī)學(xué)研究所,，他們相信這一發(fā)現(xiàn)將幫助解釋乳腺癌和病人體內(nèi)高濃度雌激素之間存在的關(guān)系。
Diamantina的癌癥生物學(xué)負(fù)責(zé)人Tom Gonda教授表示：“我們的結(jié)果證明了雌性激素打開(kāi)這一基因的能力對(duì)于乳腺癌細(xì)胞的生長(zhǎng)非常重要,。”
科學(xué)家們提到的基因被稱為MYB,，它在大約70％的乳腺癌患者體內(nèi)都存在，并且這也是數(shù)十個(gè)能促進(jìn)腫瘤生長(zhǎng)的致癌基因之一,。
Gonda教授說(shuō)：“對(duì)于乳腺癌而言,，真正重要的是雌性激素打開(kāi)MYB基因的能力，而不是基因自身發(fā)生的變異,。”他還表示小組下一步的研究計(jì)劃是將這些得到的結(jié)果在實(shí)驗(yàn)室的老鼠身上進(jìn)行測(cè)試,，之前的結(jié)果是從實(shí)驗(yàn)室分離的癌細(xì)胞上得到的，而老鼠無(wú)疑是更好的研究模型,。
Gonda教授認(rèn)為：“我們正在嘗試直接證明MYB基因能在健康的乳房組織中誘導(dǎo)出癌變,。”Gonda教授和他Queensland大學(xué)的同事和來(lái)自墨爾本、阿德萊德以及美國(guó)的科學(xué)家進(jìn)行了合作,，并將他們的發(fā)現(xiàn)發(fā)表在本周出版的著名學(xué)術(shù)刊物《Proceedings of the National Academy of Sciences of the USA》上,。Gonda表示，能阻止MYB活動(dòng)的藥物在將來(lái)或許可以用來(lái)治療乳腺癌,，但是他同時(shí)警告這還需要很長(zhǎng)時(shí)間的艱苦研究才能實(shí)現(xiàn),。
（教育部科技發(fā)展中心）
原文鏈接：http://www.physorg.com/news107176889.html
原始出處:
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
