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萊斯大學(xué)和得克薩斯大學(xué)MD安德森癌癥中心一項(xiàng)新的研究顯示了卵巢癌如何利用腹部組織來(lái)源的一種特定類(lèi)型的成體干細(xì)胞來(lái)推動(dòng)其增長(zhǎng)。這項(xiàng)研究在線(xiàn)發(fā)表在上周的Cancer Research雜志上，該研究提出了一種新的治療方式來(lái)針對(duì)侵襲性卵巢癌，即通過(guò)破壞促使癌細(xì)胞茁壯成長(zhǎng)的代謝過(guò)程。
這種特定類(lèi)型干細(xì)胞被稱(chēng)為大網(wǎng)膜脂肪基質(zhì)細(xì)胞或O-ASCs，已經(jīng)與卵巢腫瘤的增殖，遷移和耐藥性有關(guān)，但此類(lèi)干細(xì)胞的確切作用是未知的，研究論文*研究員Rice's Deepak Nagrath說(shuō)：我們發(fā)現(xiàn)，O-ASCs供給癌細(xì)胞產(chǎn)生一氧化氮所需要的代謝物，一氧化氮是已知增加血流量的重要信號(hào)分子。癌癥研究人員在80年前發(fā)現(xiàn)癌細(xì)胞與正常細(xì)胞之間的代謝差異。幾十年來(lái)，科學(xué)家相信“Warburg效應(yīng)”適用于所有的癌癥，但Nagrath實(shí)驗(yàn)室研究和其他人已經(jīng)發(fā)現(xiàn)，每一種類(lèi)型的癌癥都有自己的代謝特征。
例如，在五月發(fā)表的一項(xiàng)研究中，Nagrath及其同事發(fā)現(xiàn)高度侵襲性卵巢癌細(xì)胞是谷氨酰胺依賴(lài)性的，在實(shí)驗(yàn)室中剝奪細(xì)胞谷氨酰胺的外部來(lái)源，一些實(shí)驗(yàn)性藥物能有效殺死晚期卵巢癌細(xì)胞。
癌細(xì)胞利用腹部干細(xì)胞來(lái)推動(dòng)增長(zhǎng)和轉(zhuǎn)移。研究表明，一種新的方式即通過(guò)破壞使他們能夠茁壯成長(zhǎng)的代謝過(guò)程，來(lái)靶向治療惡性卵巢癌。在新的研究中，合著者Bahar Salimian進(jìn)行了一系列實(shí)驗(yàn)來(lái)研究O-ASCs和卵巢癌細(xì)胞之間復(fù)雜的相互作用。O-ASCs是一類(lèi)在網(wǎng)膜中發(fā)現(xiàn)的成體干細(xì)胞，網(wǎng)膜是小腹中的組織，其是卵巢癌zui常見(jiàn)的轉(zhuǎn)移部位之一。
當(dāng)我們?cè)趯?shí)驗(yàn)室共同培養(yǎng)兩種細(xì)胞類(lèi)型(癌細(xì)胞和O-ASCs)，我們發(fā)現(xiàn)，癌細(xì)胞會(huì)利用干細(xì)胞分泌的精氨酸，并且癌細(xì)胞通過(guò)燃燒精氨酸，來(lái)釋放瓜氨酸，這又造成了干細(xì)胞產(chǎn)生更多精氨酸。
我們的研究結(jié)果表明，O-ASCs通過(guò)增加一氧化氮水平，上調(diào)糖酵解和降低腫瘤細(xì)胞的氧化應(yīng)，Nagrath說(shuō)：值得注意的是，我們還發(fā)現(xiàn)在癌細(xì)胞中O-ASC介導(dǎo)的耐藥可以通過(guò)改變癌癥所依賴(lài)的一氧化氮平衡來(lái)逆轉(zhuǎn)。Nagrath說(shuō)一種破壞干細(xì)胞和腫瘤細(xì)胞之間信號(hào)的雞尾酒療法，可能破壞卵巢癌依靠的以推動(dòng)其轉(zhuǎn)移性增長(zhǎng)的代謝平衡。
每一天，你身體內(nèi)的一些細(xì)胞會(huì)停止分裂，這是一件好事。而有些細(xì)胞會(huì)無(wú)限增殖，這是大多數(shù)惡性腫瘤發(fā)展的一個(gè)重要早期步驟。
盡管細(xì)胞無(wú)限增殖在癌癥中有著非常的重要性，但研究人員一直對(duì)于細(xì)胞永生化背后的分子機(jī)制知之甚少。這是因?yàn)榭茖W(xué)家缺乏好方法研究永生化人類(lèi)細(xì)胞。在發(fā)表在Cell Cycle 雜志上的一項(xiàng)研究中，研究人員已經(jīng)開(kāi)發(fā)出一種新方法，能夠輕松地創(chuàng)建出不朽的人類(lèi)抗原抗體上皮細(xì)胞。

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【公司名稱(chēng)】 廣州健侖生物科技有限公司
【市場(chǎng)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

A new study by Rice University and the MD Anderson Cancer Center at the University of Texas shows how ovarian cancer uses a particular type of adult stem cell from abdominal tissue to drive its growth. The study, published online last week in the journal Cancer Research, suggests a new treatment for aggressive ovarian cancer, the metabolic process that promotes the robust growth of cancer cells through destruction.
This particular type of stem cell, known as omental adipose-derived stromal cells or O-ASCs, has been implicated in the proliferation, migration and drug resistance of ovarian tumors, but the exact role of such stem cells is unknown, and Rice's Deepak, lead researcher in the research paper Nagrath says: We found that O-ASCs supply the metabolites needed by cancer cells to produce nitric oxide, an important signaling molecule known to increase blood flow. Cancer researchers discovered the metabolic difference between cancer cells and normal cells 80 years ago. For decades, scientists believe the "Warburg effect" applies to all cancers, but Nagrath laboratory research and others have found that each type of cancer has its own metabolic profile.
In a study published in May, for example, Nagrath and colleagues found that highly aggressive ovarian cancer cells are glutamine-dependent, deprived of an external source of cellular glutamine in the laboratory and that some experimental drugs are effective Kill advanced ovarian cancer cells.
Cancer cells use abdomen stem cells to promote growth and metastasis. Recent research shows that a new way to target malignant ovarian cancer is by disrupting the metabolic processes that allow them to thrive. In a new study, co-author Bahar Salimian conducted a series of experiments to investigate the complex interactions between O-ASCs and ovarian cancer cells. O-ASCs are a group of adult stem cells found in the omentum, the tissue in the lower abdomen that is one of the most common metastatic sites of ovarian cancer.
When we co-cultured two cell types (cancer cells and O-ASCs) in the laboratory, we found that cancer cells utilize arginine secreted by stem cells and that cancer cells release citrulline by burning arginine, which In turn, stem cells produce more arginine.
Our results show that O-ASCs up-regulate glycolysis and reduce the oxidation of tumor cells by increasing nitric oxide levels, Nagrath said: "It is noteworthy that we have also found that O-ASC-mediated resistance in cancer cells Drugs can be reversed by altering the balance of nitric oxide on which the cancer depends. Nagrath said a cocktail of drugs that disrupt the signal between stem cells and tumor cells could destroy the metabolic balance that ovarian cancer depends on to promote its metastatic growth.
Every day, some cells in your body will stop dividing, which is a good thing. While some cells proliferate indefiniy, this is an important early step in the development of most malignancies.
Despite the extraordinary importance of cell immortalization in cancer, researchers have long known little about the molecular mechanisms behind the immortalization of cells. This is because scientists lack a good way to study immortalized human cells. In a study published in the journal Cell Cycle, researchers have developed a new way to easily create immortal human antigen-antibody epithelial cells.