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UT西南醫(yī)學(xué)中心細(xì)胞生物學(xué)副主席Jerry W. Shay教授及其同事、細(xì)胞生物學(xué)和內(nèi)科醫(yī)學(xué)教授Woodring E. Wright發(fā)現(xiàn)，6-thio-2'-脫氧鳥苷(6-thio-2'-deoxyguanosine)能阻止培養(yǎng)物中癌細(xì)胞的生長，并減少小鼠體內(nèi)腫瘤的生長。
Harold C. Simmons 綜合癌癥中心副主任Shay博士說：“我們觀察到，用很低濃度的6-thiodG，就能有效地對(duì)抗一系列癌細(xì)胞系，并且減輕小鼠體內(nèi)的腫瘤負(fù)荷。”
相關(guān)研究結(jié)果發(fā)表在zui近的*學(xué)術(shù)期刊《Cancer Discovery》，本文共同資深作者是Shay和Wright博士。
6-thiodG通過靶定一種*的機(jī)制而發(fā)揮作用，這種機(jī)制被認(rèn)為可調(diào)節(jié)細(xì)胞的存活時(shí)間，是一種衰老時(shí)鐘。這種生物鐘被定義為一種DNA結(jié)構(gòu)，稱為端粒，其位于細(xì)胞染色體末端，可保護(hù)染色體不受傷害，每當(dāng)細(xì)胞分裂時(shí)它就會(huì)縮短。一旦端粒縮短到臨界長度，細(xì)胞就不再分裂，并通過一個(gè)稱為細(xì)胞凋亡的過程死亡。
癌細(xì)胞通過一個(gè)稱為端粒酶的RNA蛋白質(zhì)復(fù)合物，免于這種死亡，端粒酶可確保端粒在每次細(xì)胞分裂時(shí)不會(huì)縮短。端粒酶也因此成為眾多癌癥治療靶標(biāo)研究的目標(biāo)。成功阻斷端粒酶活性的藥物已經(jīng)開發(fā)出來，但是這些藥物要使用很長一段時(shí)間，以成功地觸發(fā)細(xì)胞死亡和縮減腫瘤，從而會(huì)導(dǎo)致相當(dāng)大的毒性。這樣的預(yù)后結(jié)果部分是因?yàn)椋魏我粋€(gè)腫瘤中的細(xì)胞，其染色體具有不同的端粒長度，任何一個(gè)細(xì)胞的端粒酶必須慎重被縮短以誘導(dǎo)死亡。
6-thiodG優(yōu)先被用作端粒酶的一種底物，可破壞細(xì)胞保持端粒長度的正常方式。因?yàn)?-thiodG通常不用于端粒，因此該化合物的存在，就作為一種“警告”信號(hào)，細(xì)胞將其識(shí)別為損傷。因此，細(xì)胞就停止分裂并死亡。
端粒酶是一種幾乎通用的腫瘤靶標(biāo)，但是研究人員指出，少有端粒酶療法進(jìn)入人體臨床試驗(yàn)。
Wright博士說：“在這一點(diǎn)上，利用端粒酶將有毒產(chǎn)物整合進(jìn)端粒，是非常鼓舞人心的。”
重要的是，和其他許多端粒酶抑制化合物不同，研究人員并沒有在6-thiodG治療小鼠的血液、肝臟和腎臟中觀察到嚴(yán)重的副作用。
Shay博士說：“由于端粒酶在幾乎所有的人類腫瘤中表達(dá)，這項(xiàng)工作提出了一種潛在創(chuàng)新的方法，靶定端粒酶表達(dá)的癌細(xì)胞，而對(duì)正常細(xì)胞的毒副作用較小。我們相信這種小分子將填補(bǔ)未知領(lǐng)域中的一個(gè)未曾滿足的癌癥需要，將被迅速應(yīng)用于臨床。”

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【公司名稱】 廣州健侖生物科技有限公司
【市場部】    楊永漢

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【騰訊  】 2042552662
【公司地址】 廣州清華科技園創(chuàng)新基地番禺石樓鎮(zhèn)創(chuàng)啟路63號(hào)二期2幢101-103室

Jerry W. Shay, vice president of cell biology at UT Southwestern Medical Center and his colleague Woodring E. Wright, professor of cellular and medical science, found that 6-thio-2'-deoxyguanosine ) Can prevent the growth of cancer cells in culture and reduce the growth of tumors in mice.
"We observed that with a very low concentration of 6-thiodG, we were able to effectively fight a series of cancer cell lines and reduce the tumor burden in mice," said Dr. Shay, associate director of the Harold C. Simmons Comprehensive Cancer Center.
Relevant research results published in the recent top international academic journals Cancer Discovery, co-senior author of this article are Dr. Shay and Wright.
6-thiodG works by targeting a unique mechanism that is thought to regulate cell survival and is an aging clock. This biological clock is defined as a DNA structure called a omere located at the end of a cell's chromosome that protects the chromosome from harm and shortens it whenever the cell divides. Once the omere has shortened to a critical length, the cells no longer divide and die through a process called apoptosis.
Cancer cells pass through an RNA protein complex called omerase, which is immune from this death, and omerase ensures that omeres will not shorten each cell division. omerase has therefore become the target of numerous cancer therapy targets. Drugs that successfully block omerase activity have been developed, but these drugs have been used for a long time to successfully trigger cell death and shrink tumors, resulting in considerable toxicity. This prognosis is due in part to the fact that the cells in any one tumor have different omere lengths on their chromosomes and the omerase in any one cell must be carefully shortened to induce death.
6-thiodG is preferentially used as a substrate for omerase and can disrupt the normal way in which cells retain omere length. Because 6-thiodG is not normally used for omeres, the presence of this compound serves as a "warning" signal that cells recognize as damaging. As a result, the cells stop dividing and die.
omerase is an almost universal tumor target, but researchers point out that few omerase therapies enter human clinical trials.
Dr. Wright said: "At this point, the use of omerase to integrate toxic products into omeres is very encouraging."
Importantly, unlike many other omerase inhibiting compounds, the researchers did not observe serious side effects in the blood, liver and kidneys of 6-thiodG-treated mice.
Dr. Shay said: "Since omerase is expressed in almost all human tumors, this work presents a potentially innovative approach that targets omerase-expressing cancer cells with less toxic side effects on normal cells. We believe that such small molecules will fill an unmet need for cancer in an unknown area and will be rapidly applied to the clinic. "