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EIKEN軍團(tuán)菌快速檢測(cè)試劑盒

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【公司名稱(chēng)】 廣州健侖生物科技有限公司
【】    楊永漢 
【】 
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【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101-3室
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美國(guó)在肺癌治療上的花費(fèi)超過(guò)120億美元。然而，肺癌的存活率不容樂(lè)觀，由于疾病極易轉(zhuǎn)移到整個(gè)身體，有80%的患者在診斷后5年之內(nèi)死亡。
為了獲得轉(zhuǎn)移性，癌細(xì)胞會(huì)覆蓋一般保持細(xì)胞根植在它們各自位置的細(xì)胞器。癌癥可以迂回地打開(kāi)和關(guān)閉細(xì)胞膜上突起的分子錨(稱(chēng)為附著斑復(fù)合物)，為遷移準(zhǔn)備細(xì)胞。這使得癌細(xì)胞開(kāi)始經(jīng)過(guò)血流遍歷體內(nèi)，在新的器官駐留下來(lái)。
除了不同的癌癥能控制這些錨之外，大約五分之一的肺癌病例缺失一個(gè)抗癌基因，稱(chēng)為L(zhǎng)KB1(又名STK11)。缺失LKB1的癌癥通常是侵襲性的，可在體內(nèi)迅速蔓延。然而，沒(méi)有知道LKB1和粘附斑之間是如何關(guān)聯(lián)的。
現(xiàn)在，索爾克研究小組發(fā)現(xiàn)了這個(gè)關(guān)聯(lián)，并發(fā)現(xiàn)了一個(gè)新的治療靶點(diǎn)：一個(gè)鮮為人知的基因，稱(chēng)為DIXDC1。研究人員發(fā)現(xiàn)，DIXDC1接受來(lái)自L(fǎng)KB1的指令，轉(zhuǎn)到粘著斑，并改變它們的數(shù)量和大小。
當(dāng)DIXDC1被“打開(kāi)”，半打左右的粘著斑變大并具有粘性，將細(xì)胞錨定在它們的位置。當(dāng)DIXDC1被阻斷或滅活時(shí)，粘著斑變小和量大，導(dǎo)致數(shù)百只小“手”向前拉動(dòng)細(xì)胞，以響應(yīng)細(xì)胞外的線(xiàn)索。轉(zhuǎn)移的傾向增加，有助于癌細(xì)胞從肺部逃跑，可讓腫瘤細(xì)胞存活下來(lái)，經(jīng)過(guò)血液并停留在體內(nèi)各處的器官。
本研究*作者、博士研究生Jonathan Goodwin稱(chēng)：“LKB1和DIXDC1之間的交流可引起細(xì)胞內(nèi)的一種‘鎖定(stay-put)’信號(hào)。人們了解較少的DIXDC1，在癌癥和轉(zhuǎn)移中原來(lái)是被抑制的。”
Shaw和同事在新的研究中發(fā)現(xiàn)，腫瘤有兩種方法來(lái)關(guān)閉這個(gè)“鎖定”信號(hào)。一是通過(guò)直接抑制DIXDC1。另一種方法是通過(guò)刪除LKB1，然后不再給DIXDC1發(fā)信號(hào)轉(zhuǎn)到粘著斑錨定細(xì)胞。鑒于此，科學(xué)家們想知道，是否復(fù)活DIXDC1就能停止癌癥的轉(zhuǎn)移。他們獲取了轉(zhuǎn)移細(xì)胞，這些細(xì)胞具有低水平的DIXDC1，并在細(xì)胞中過(guò)度表達(dá)這個(gè)基因。DIXDC1的加入，確實(shí)在體內(nèi)和體外削弱了這些細(xì)胞的轉(zhuǎn)移能力。
Goodwin稱(chēng)：“這非常非常的奇怪，這個(gè)基因會(huì)如此強(qiáng)大。在這項(xiàng)研究開(kāi)始時(shí)，我們也不知道DIXDC1會(huì)參與轉(zhuǎn)移。LKB1會(huì)影響許多蛋白質(zhì);單*個(gè)基因控制如此多的表型，是我們沒(méi)有預(yù)料到的。”
現(xiàn)在，對(duì)具有LKB1或DIXDC1改變的癌癥，還沒(méi)有特定的治療方法，但是具有這些基因缺失的癌癥，可以通過(guò)靶定粘著斑的癌癥藥物得以治療。

The United States spends more than 12 billion U.S. dollars on lung cancer treatment. However, the survival rate of lung cancer is not optimistic, as the disease easily transferred to the entire body, 80% of patients died within 5 years after diagnosis.
In order to obtain metastaticity, cancer cells will cover organelles that generally keep the cells rooted in their respective locations. Cancers roundaboutly open and close protruding molecular anchors (called attachment plaque complexes) on the cell membrane, preparing cells for migration. This allows cancer cells to start traversing the bloodstream and residing in new organs.
In addition to the fact that different cancers can control these anchors, about one in five lung cancers lack an anti-cancer gene, called LKB1 (aka STK11). Cancers that lack LKB1 are usually aggressive and spread rapidly in the body. However, it is not known how LKB1 and adhesive spots are related.
Now, the Sork study found the link and found a new therapeutic target: a little-known gene called DIXDC1. The researchers found that DIXDC1 received instructions from LKB1, turned to sticky patches, and changed their number and size.
When DIXDC1 is "on", about half a dozen sticky patches become large and sticky, anchoring the cells in their place. When DIXDC1 is blocked or inactivated, the sticky patches become small and large, causing hundreds of small "hands" to pull the cells forward in response to extracellular cues. The increased tendency to metastasize helps the cancer cells escape from the lungs, allowing the tumor cells to survive, pass through the blood and remain in the organs throughout the body.
Jonathan Goodwin, Ph.D., lead author and lead author of the study, said: "The exchange between LKB1 and DIXDC1 causes a 'stay-put' signal in the cell.It has been known that less DIXDC1 is found in cancers and metastases Is suppressed. "
In a new study, Shaw and colleagues found that tumors have two ways to turn off this "lock" signal. First, by directly inhibiting DIXDC1. Another approach is by deleting LKB1 and then no longer signaling DIXDC1 to focal adhesion cells. In view of this, scientists wondered whether the resumption of DIXDC1 would halt the metastasis of cancer. They acquired metastatic cells that had low levels of DIXDC1 and over-expressed the gene in the cell. The addition of DIXDC1 does indeed weaken the metastatic capacity of these cells in vivo and in vitro.
"It's very, very strange, this gene is so powerful, and at the start of the study we did not know that DIXDC1 would be involved in the transfer, LKB1 affects many proteins, and controlling so many phenotypes by a single gene is what we Unexpectedly. "
There are no specific treatments for cancers with changes in LKB1 or DIXDC1, but cancers with these gene deletions can now be treated with cancer drugs that target focal adhesions.