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【置顶】抗氧化剂的抑制作用能够清除胰腺癌细胞

2016-08-03 00:00


Antioxidant suppression eradicates pancreatic cancer cell
抗氧化剂的抑制作用能够清除胰腺癌细胞


 

A novel drug therapy - that mimics the suppression of an antioxidant-promoting protein - kills pancreatic cancer cells, new research reveals.
一种新的研究揭示了,有一种新的药物治疗——模拟抗氧化剂的抑制作用——促进蛋白——能够杀死胰腺癌细胞。

According to the American Cancer Society, around 53,070 people will be diagnosed with pancreatic cancer in the Unites States in 2016, and around 41,780 people will die of the disease. Pancreatic cancer accounts for about 3 percent of all cancers in the U.S. and about 7% of cancer deaths.
根据美国癌症学会的数据,2016年,在美国越有53070名患者被确证为胰腺癌,有41780位患者死于该病。在美国,胰腺癌约占所有癌症的3%,以及占癌症死亡的7%。

Pancreatic cancer is caused by the abnormal, uncontrolled growth of cells in the pancreas.
A research team at Cold Spring Harbor Laboratory (CSHL) in New York finds that reducing levels of antioxidants in pancreatic cells can help to kill them. This new strategy for eradicating pancreatic cancer cells may open new doors for treating this serious illness, in which less than 5 percent of patients survive 5 years.
胰腺癌是由胰腺细胞变异、不受控制生长而造成的。位于纽约的冷泉港实验室(CSHL)的一只研究小组发现,减少胰腺细胞中抗氧化剂的水平能够帮助杀死他们。这个清除胰腺癌细胞的新策略,为治疗这种恶性疾病打开了新世界的大门。须知道,这种罹患这种疾病的患者5年存活率低于5%。

"Antioxidant" has become a popular buzzword that is viewed as a cure-all notion for health ailments; it is widely believed that raising levels of antioxidants stops cancer cells from developing.
“抗氧化剂”已成为一个能治愈所有疾病的热词;大家都认为抗氧化剂水平的提高有利于阻止癌细胞的增长。

In reality, although antioxidants interact with and neutralize free radicals and prevent them from causing damage, there is little available evidence that antioxidants prevent cancer.
实际上,尽管抗氧化剂同游离基之间会产生反应且能中和自由基,也可以阻止其产生损害,但几乎没有证据证明抗氧化剂能阻止癌症。

Furthermore, trials have found that people taking antioxidant supplements during cancer therapy have worse outcomes, especially if they were smokers.
而且,实验表明患者在治疗癌症期间服用抗氧化剂产生的效果可能更糟,尤其是吸烟人群。

Does increasing antioxidant levels do more harm than good?
增加抗氧化剂的水平弊大于利吗?

In a series of complex experiments, the CSHL researchers demonstrate that in pancreatic cells that are abnormal or in a malignant state, raising antioxidant levels can do more harm than good.
在一系列的复杂实验中,CSHL的研究者展示说在胰腺非正常细胞或恶性细胞中增加抗氧化剂的水平造成的损害大于益处。

In healthy cells, the amounts of oxidizing and anti-oxidizing agents are kept precisely balanced in every cell.
在健康细胞中,每个细胞中氧化和抗氧化物质保持着精确的平衡。

However, in proliferating cancer cells - that are increasing rapidly in number through growth and cell pision - the amounts of oxidants in malignant cells increase, but anti-oxidants also increase to counter the impact of rising oxidation.
然而,在增殖的癌细胞中——通过细胞生长和细胞分裂在数量上迅速增长——恶性细胞中氧化剂的数量是在增长的,同时抗氧化剂也在增长,来对氧化剂增长所带来的冲击。

CSHL's Prof. David Tuveson - M.D., Ph.D., director of research for the Lustgarten Foundation - and colleagues note that without the amounts of antioxidants going up in scale with the oxidants, malignant cells will die from excessive oxidation.
CSHL教授David Tuveson – M.D.、Ph.D.、勒斯特加滕基金会研究主任 – 和他的同事们注意到,如果抗氧化剂的数量没有同氧化剂成比例地增长,恶性细胞会因为氧化剂过量而死亡。

"Of course, that's exactly what we want cancer cells to do - to burn themselves out," says Iok In Christine Chio, a postdoctoral investigator in the Tuveson lab who led the experiments.
博士后研究员,也是勒斯特加滕实验室项目带头人Iok In Christine Chio说“当然,这正是我们试图让癌细胞发生的动作 – 将它自己烧死。”

"The therapeutic principle our lab is testing is whether, by increasing the level of oxidation in cancer cells, we can cause pre-malignant and malignant cells to die," she adds.
她还说:“我们在实验室的治疗原则是,测试在恶性细胞中增加氧化剂的数量能否导致恶性细胞或将要恶化的细胞死亡。”

Excessive oxidation causes cells to commit suicide
过量的氧化剂可使细胞自杀

Treatments for cancer such as radiation therapy and chemotherapy destroy cancer cells by promoting oxidation. Although antioxidants protect cellular DNA from damage by oxidative stress, they likely protect cancer cells, too.
放疗和化疗都是通过促使细胞中的氧化剂增量来消灭癌细胞的。尽管抗氧化剂能够通过氧化应激反应来保护细胞核中的DNA不受损害,但它同时也可以保护癌细胞。

Exposing cells to excessive oxidation causes them to experience programmed cell death called apoptosis. A method of increasing oxidation in cancer cells is to decrease levels of antioxidants within the same cells.
将细胞暴露给氧化剂可使其按一定程序死亡的过程叫细胞凋亡。有一种增加癌细胞中氧化剂的方法就是降低同一细胞中抗氧化剂的水平。

Tuveson and team aimed to find a technique whereby they could increase oxidation without harming healthy cells. They concentrated on NRF2, a protein that can be tweaked to disrupt the balance between oxidation and decreased cancer cells.
Tuveson和他的团队的研究目的就是,找到一种能够增加氧化剂还不伤害健康细胞的技术。他们将注意力集中在NRF2上,一种能够通过微调来打乱氧化剂间平衡,从而减少癌细胞的蛋白。

When NRF2 is active, cells synthesize a chemical called glutathione, an important antioxidant. However, it is not possible to reduce NRF2 activity or make it inactive, as it has a role in regulating several hundred different genes. "One can't delete it from a cell without impacting many other processes," says Chio.
当NRF2活跃时,细胞能合成一种化学物质叫谷胱甘肽,一种重要的抗氧化剂。然而,想要减少NRF2的活性或使其失活是不可能的,因为这种蛋白需要调节几百种基因。Chio说“如果试图将这种蛋白从细胞中删除又不影响其它作用是不可能的。”

The team used samples of pancreas cells from people with pancreatic cancer (malignant and pre-malignant) and inpiduals with a healthy pancreas to conduct an experiment where NRF2 was eliminated.
研究团队用在胰腺癌患者身上提取的胰腺细胞(患病细胞和将患病细胞)和健康人身上提取的胰腺细胞做了实验,将NRF2从中排除。

Normal pancreas cells not harmed by two-drug treatment
正常胰腺细胞不会被两种药物联和治疗损害

They found that when NRF2 was missing, the process of translating messages from the genes into proteins was highly affected by the oxidant and antioxidant balance, but only in the cancerous cells. The healthy cells were still able to produce the proteins.
他们发现当NRF2消失时,将基因信息翻译变成蛋白质的过程在很大程度上受氧化剂和抗氧化剂之间平衡的影响,但仅限于癌细胞。正常的健康细胞仍然能产生蛋白。

"We were very excited when we saw this. This meant that if we could find a way of reducing antioxidants, protein synthesis would only be impacted in precancerous and malignant cells, a potentially powerful therapeutic strategy."
“我们发现这点后特别兴奋。这意味着,如果我们有办法减少抗氧化剂的量,蛋白质合成只在癌症前期细胞和患病细胞中受影响,这是一种潜力很大的治疗方法。”

The crux of the experiment was to use two drugs in combination: an AKT (protein kinase B) inhibitor, and a BSO (buthionine sulfoximine), which reduces levels of glutathione.
实验的核心是两种药物联用:一种AKT(蛋白质激酶B)抑制剂,和一种BSO(丁硫氨酸亚砜胺),可以减少谷胱甘肽的水平。

AKT inhibitors have been used in trials on cancer patients before but with limited success. The team wanted to combine this with the BSO to mimic what would happen if they could reduce levels of NRF2.
AKT抑制剂以前在癌症患者身上做过实验,但效果有限。研究团队试图将其同BSO联用,如果在他们能减少NRF2水平的情况下,看能发生什么情况。


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