盡管人們已經(jīng)知道,，食用綠色花椰菜（broccoli）、黃白色花椰菜（cauliflower）,、卷心菜等十字花科蔬菜可以預防癌癥,，但它們具體的抗癌機制卻不清楚。
近日,，美國加利福尼亞大學圣巴巴拉分校的生化與藥理學教授萊斯利·威爾遜（Leslie Wilson）和該校分子細胞與發(fā)育生物學系的副教授瑪麗·安·喬丹（Mary Ann Jordan）在國際著名學術雜志《癌癥發(fā)生》（Carcinogenesis）上發(fā)表文章,，闡明了十字花科蔬菜的抗癌機制。
這篇文章的第一作者,、威爾遜教授的研究生奧爾加·阿扎倫科（Olga Azarenko）指出：“在所有癌癥中,，乳癌的致死率排名第二。但食用十字花科蔬菜（如卷心菜）可預防這種癌癥,，這是為什么呢,？經(jīng)過我們的研究發(fā)現(xiàn)，在這類蔬菜中,，含有一種具有預防和抗癌活性的化學物質硫氰酸鹽（isothiocyanate）,。在綠色和黃白色花椰菜中，這類化學物質的含量是最高的。”
阿扎倫科補充說：“我們的文章主要討論了硫氰酸鹽的抗癌活性,。在研究中,，這類物質已經(jīng)表現(xiàn)出較強的抗癌能力，可以降低實驗動物的癌癥發(fā)生率,。另外,，它們還能抑制人類乳癌細胞的生長，甚至殺死癌細胞,。”
阿扎倫科驚奇地發(fā)現(xiàn),，硫氰酸鹽一直人類癌細胞的方式居然與抗癌藥物紫杉醇（taxol）和長春新堿（vincristine）很相似：都是抑制細胞的有絲分裂（對于正常細胞而言，有絲分裂是細胞分裂的重要過程,。在這一過程中,，染色體會進行復制并準確分配到兩個子細胞中）。
在有絲分裂階段,，細胞內會有大量微小的管狀物質（即微管,，microtubule），它們將幫助細胞把兩套染色體分開（一套是原來的,，另一套是復制形成的）,。與很多來自于其他植物的抗癌物質類似，硫氰酸鹽也是抑制干擾微管的功能,，從而阻止有絲分裂的正常進行,。與其他抗癌藥物相比，硫氰酸鹽的毒性更低,。
威爾遜教授說：“硫氰酸鹽可能是一種很有效的癌癥預防藥物,，因為它能阻止癌細胞增殖，并殺死癌變細胞,。”此外,，硫氰酸鹽還可與紫杉醇等抗癌藥物聯(lián)用，以增強抗癌效果,，而且不會加重藥物毒性,。（生物谷Bioon.com）
生物谷推薦原始出處：
Carcinogenesis 2008 29(12):2360-2368; doi:10.1093/carcin/bgn241
Suppression of microtubule dynamic instability and turnover in MCF7 breast cancer cells by sulforaphane
Olga Azarenko, Tatiana Okouneva, Keith W. Singletary1, Mary Ann Jordan and Leslie Wilson*
Department of Molecular, Cellular, and Developmental Biology and the Neuroscience Research Institute, University of California, Santa Barbara, CA 93106, USA
1 Department of Food Science and Human Nutrition, University of Illinois, Urbana, IL 61801, USA
Sulforaphane (SFN), a prominent isothiocyanate present in cruciferous vegetables, is believed to be responsible along with other isothiocyanates for the cancer preventive activity of such vegetables. SFN arrests mitosis, possibly by affecting spindle microtubule function. A critical property of microtubules is their rapid and time-sensitive growth and shortening dynamics (dynamic instability), and suppression of dynamics by antimitotic anticancer drugs (e.g. taxanes and the vinca alkaloids) is central to the anticancer mechanisms of such drugs. We found that at concentrations that inhibited proliferation and mitosis of MCF7-green fluorescent protein--tubulin breast tumor cells by 50% (15 μM), SFN significantly modified microtubule organization in arrested spindles without modulating the spindle microtubule mass, in a manner similar to that of much more powerful antimitotic drugs. By using quantitative fluorescence video microscopy, we determined that at its mitotic concentration required to inhibit mitosis by 50%, SFN suppressed the dynamic instability of the interphase microtubules in these cells, strongly reducing the rate and extent of growth and shortening and decreasing microtubule turnover, without affecting the polymer mass. SFN suppressed the dynamics of purified microtubules in a similar fashion at concentrations well below those required to depolymerize microtubules, indicating that the suppression of dynamic instability by SFN in cells is due to a direct effect on the microtubules. The results indicate that SFN arrests proliferation and mitosis by stabilizing microtubules in a manner weaker than but similar to more powerful clinically used antimitotic anticancer drugs and strongly support the hypothesis that inhibition of mitosis by microtubule stabilization is important for SFN's chemopreventive activity.
