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【medical-news】HIV蛋白参与辅助杀伤癌症细胞
2/15/2007
HIV蛋白参与辅助杀伤癌症细胞
Source: Washington University School of Medicine
来源：华盛顿大学医学校
Cancer cells are sick, but they keep growing because they don't react to internal signals urging them to die. Now researchers at Washington University School of Medicine in St. Louis have found an efficient way to get a messenger into cancer cells that forces them to respond to death signals. And they did it using one of the most sinister pathogens around — HIV.
癌症细胞是病态的，但它们对体内的促使死亡信号无反应，因此可以持续生长。位于圣-路易斯的华盛顿大学医学校的研究者目前发现一个能够进入癌症细胞的有效的信使，它能够迫使癌症细胞对死亡信号起反应。并且他们应用了最可怕的病原体HIV来实现了其目的。
"HIV knows how to insert itself into many different types of cells," says senior author William G. Hawkins, M.D., assistant professor of surgery and a member of the Siteman Cancer Center at the School of Medicine and Barnes-Jewish Hospital. "A portion of the HIV protein called TAT can transport biologically active compounds into cells. TAT is small, but it can move massive molecules. You could almost hook TAT up to a train, and TAT would drag it inside a cell. So we've taken advantage of this ability."
来自Barnes-Jewish医院，医学校Siteman癌症中心的成员，外科学副教授，文章的高级作者，William G. Hawkins博士说：“HIV能够插入许多种不同类型的细胞，其TAT蛋白的一部分能够转运生物活性物质进入细胞。TAT本身很小，但它却能够转运大分子。你几乎可以给TAT挂一辆火车，TAT将把它拖进细胞内。因此，我们应用了它的这一能力。”
In an article published online in January 2007 in the Annals of Surgical Oncology, the researchers describe using TAT to pull a protein called Bim into cancer cells. TAT alone cannot cause AIDS and has no adverse health effects. Bim acts as a tumor suppressor and causes cancer cells to die through apoptosis, a process by which cells "commit suicide."
在2007年1月外科肿瘤学年鉴在线发表的一篇文章中，研究者应用TAT将名为Bim的蛋白拉入癌症细胞。TAT自身不会导致艾滋病，对健康无害。Bim作为一种肿瘤抑制物能够引起癌症细胞凋亡，该过程又叫做细胞“自杀”。
The research team found that the TAT-Bim compound activated apoptosis mechanisms in cancer cells and augmented the cell-killing effect of radiation. When mice with malignant tumors were treated with TAT-Bim, their tumors shrank, and they survived longer than mice that didn't get the treatment. After 40 days, 80 percent of mice receiving TAT-Bim were alive compared to 20 percent of mice that didn't get the treatment.
研究小组发现，TAT-Bim复合物激活癌症细胞凋亡的机制和增强细胞杀伤效应。当应用TAT-Bim复合物处理有恶性肿瘤的小鼠后，小鼠肿瘤缩小，存活时间较不处理组小鼠长。40日后，处理组小鼠80％存活，而未处理组仅有20％存活。
Hawkins asserts that this success marks the beginning of a very promising new approach to cancer therapy. "This is the tip of the iceberg," he says. "Now that we've proven we can do this, we've started creating a battery of proteins that can push cancer cells to die."
Hawkins断言，这项成功将标志着一种非常有前景的新的癌症肿瘤肿瘤方法的诞生。他说：“这只是冰山的一角，现在我们已经证实我们能够作这件事，我们已经开始创造一系列蛋白试验来促使癌症细胞死亡。”
Hawkins says he thinks treatments that activate apoptosis mechanisms could provide new options for patients with the deadliest cancers — such as pancreatic cancer — which have very low rates of survival. He says he believes that clinical trials of these compounds could be just a few years away.
Hawkins 说，他认为这种激活凋亡机制的治疗能够给死亡线上的癌症患者，如存活率极低的胰腺癌患者，提供一种新的选择。他说，他相信这些混合物的临床试验将在近几年之后进行。
Hawkins began researching TAT-Bim after discussions with co-author Richard S. Hotchkiss, M.D., professor of anesthesiology, medicine and surgery and associate professor of molecular biology and pharmacology. Hotchkiss was seeking proteins that inhibit apoptosis in patients with life-threatening infections and found that TAT-Bim had the unwanted effect of increasing cell death. Hawkins wondered if TAT-Bim could be effective against cancer, and a productive scientific collaboration began between their labs to exploit the anticancer potential of TAT-Bim.
Hawkins 在与生物学和药理学副教授，麻醉学、内科学和外科学教授，文章的共同作者，Richard S. Hotchkiss博士讨论后，便开始研究TAT-Bim。Hotchkiss当时正在寻找能够抑制致命性感染患者凋亡的蛋白，他发现TAT-Bim有增加细胞死亡的效应。Hawkins想知道，TAT-Bim复合物是否能够有效的抑制癌症，从而在他们的实验室之间建立了有效的科学合作来探索TAT-Bim的潜在抗癌能力。
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作者:admin@医学,生命科学 2011-03-05 05:27
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