近日,，一項(xiàng)刊登在國(guó)際雜志Laboratory Investigation上的研究論文中,，來(lái)自堪薩斯城退伍軍人醫(yī)療中心的研究人員通過(guò)研究發(fā)現(xiàn)，每日服用一定的劑量的阿司匹林或可有效阻斷乳腺癌的生長(zhǎng),，此前研究顯示阿司匹林或許對(duì)結(jié)腸癌,、胃腸道癌、前列腺癌等其它癌癥均有一定的抑制作用,。
Banerjee教授說(shuō)道,，在癌癥治療前期階段一旦盡力去治療患者，一般腫瘤都會(huì)有希望被有效遏制住,，但由于癌癥干細(xì)胞的存在,，其往往會(huì)對(duì)化療或其他癌癥療法產(chǎn)生耐受性，從而在機(jī)體深入開(kāi)始休眠，一旦機(jī)體條件合適癌癥干細(xì)胞就會(huì)死灰復(fù)燃,，因此當(dāng)癌癥干細(xì)胞重新被激活增殖時(shí),，癌癥就會(huì)變得難以對(duì)付。
為了檢測(cè)阿司匹林是否可以改變?nèi)橄侔┘?xì)胞的分子特性而使其不再擴(kuò)散,，研究者利用培養(yǎng)中的細(xì)胞和小鼠模型進(jìn)行研究,；研究者將乳腺癌細(xì)胞置于96孔板中進(jìn)行孵育培養(yǎng)，給其中一半的培養(yǎng)液中加入阿司匹林,，隨后研究者發(fā)現(xiàn)阿司匹林可以明顯增加所檢測(cè)細(xì)胞的死亡率,，而沒(méi)有死亡的細(xì)胞中也有很多細(xì)胞生長(zhǎng)發(fā)生了延遲。
隨后研究者對(duì)20只患惡性腫瘤的小鼠進(jìn)行研究,，在15天的研究時(shí)間里,，研究者每日給予其中一半的小鼠和人類相同劑量的阿司匹林，即75毫克（被認(rèn)為是最低劑量）,，在研究結(jié)束時(shí),，對(duì)小鼠機(jī)體中的腫瘤進(jìn)行稱重，結(jié)果發(fā)現(xiàn),，接受阿司匹林的小鼠的腫瘤平均重量減少了47%,。
為了揭示阿司匹林可以抑制癌癥，研究者們?cè)陬~外的一組小鼠暴露于癌細(xì)胞之間給其施用阿司匹林,，15天后相比對(duì)照組小鼠而言,，這些小鼠機(jī)體腫瘤的癌性生長(zhǎng)明顯降低了；研究者說(shuō)道,，我們發(fā)現(xiàn)阿司匹林可以促使機(jī)體殘留的癌細(xì)胞失去自我更新的能力,，從本質(zhì)上來(lái)講這些癌細(xì)胞將不能夠生長(zhǎng)或再生。因此如果在化療后給予患者一定的阿司匹林或可有效抑制患者機(jī)體癌癥的復(fù)發(fā),，從而為改善患者的預(yù)后和生活質(zhì)量提供一定的幫助,。
專家們建議患者在服用阿司匹林之前咨詢一下醫(yī)生，因?yàn)檫@種藥物可以稀釋血液并且增加腸道出血的風(fēng)險(xiǎn),，當(dāng)然阿司匹林存在一定的風(fēng)險(xiǎn),，但我們也不得不衡量一下其可以抵御癌癥的效用；后期研究者將會(huì)進(jìn)行更多的研究來(lái)闡明阿司匹林抑制癌癥發(fā)展的機(jī)理,，該研究為有效改善癌癥患者的健康以及開(kāi)發(fā)預(yù)防癌癥復(fù)發(fā)的策略將提供一定的研究基礎(chǔ)和線索,。
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doi:10.1038/labinvest
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Aspirin blocks growth of breast tumor cells and tumor-initiating cells and induces reprogramming factors of mesenchymal to epithelial transition.
Maity G1, De A2, Das A1, Banerjee S3, Sarkar S4, Banerjee SK5.
Acetylsalicylic acid (ASA), also known as aspirin, a classic, nonsteroidal, anti-inflammatory drug (NSAID), is widely used to relieve minor aches and pains and to reduce fever. Epidemiological studies and other experimental studies suggest that ASA use reduces the risk of different cancers including breast cancer (BC) and may be used as a chemopreventive agent against BC and other cancers. These studies have raised the tempting possibility that ASA could serve as a preventive medicine for BC. However, lack of in-depth knowledge of the mechanism of action of ASA reshapes the debate of risk and benefit of using ASA in prevention of BC. Our studies, using in vitro and in vivo tumor xenograft models, show a strong beneficial effect of ASA in the prevention of breast carcinogenesis. We find that ASA not only prevents breast tumor cell growth in vitro and tumor growth in nude mice xenograft model through the induction of apoptosis, but also significantly reduces the self-renewal capacity and growth of breast tumor-initiating cells (BTICs)/breast cancer stem cells (BCSCs) and delays the formation of a palpable tumor. Moreover, ASA regulates other pathophysiological events in breast carcinogenesis, such as reprogramming the mesenchymal to epithelial transition (MET) and delaying in vitro migration in BC cells. The tumor growth-inhibitory and reprogramming roles of ASA could be mediated through inhibition of TGF-β/SMAD4 signaling pathway that is associated with growth, motility, invasion, and metastasis in advanced BCs. Collectively, ASA has a therapeutic or preventive potential by attacking possible target such as TGF-β in breast carcinogenesis.
