Researchers found the survival mechanism of cancer cells
November 24, 2016 Source: Bio Valley
Window._bd_share_config={ "common":{ "bdSnsKey":{ },"bdText":"","bdMini":"2","bdMiniList":false,"bdPic":"","bdStyle":" 0","bdSize":"16"},"share":{ }};with(document)0[(getElementsByTagName('head')[0]||body).appendChild(createElement('script')) .src='http://bdimg.share.baidu.com/static/api/js/share.js?v=89860593.js?cdnversion='+~(-new Date()/36e5)];International research led by scientists from the London Creek Institute and the Hebrew University of Jerusalem reveals the mechanisms of survival in cancer cells, which can erupt again even after aggressive treatment. In a paper published in Science (LINK), the researchers described the mechanism by which cancerous tumor cells become cancer stem cells that can sustain long-term growth.
As cancer develops, the resulting cells are not uniform in their biological properties and contribute differently to tumor development. Only a small percentage of cancer cells can form new tumors or metastases, which are called "cancer stem cells." This difference between tumor cells constitutes a major challenge in understanding the nature of the tumor, its sensitivity to drugs, and the effective treatment of planning to eliminate all tumor cells.
Professor Eran Meshorer, director of the Stem Cell and Epigenetics Laboratory at the Institute of Life Sciences, said: "Many chemotherapy drugs leave a small amount of cancer stem cells, causing the disease to re-emerge after a few years. Therefore, it is important to identify cancer stem cells in tumors. And characterize the differences between different tumor cells as the basis for the detection of weaknesses in the development of the disease."
Cancer stem cells are not limited to the tumor itself, they are able to participate again in the healthy environment and stimulate the disease. To study the characteristics of these unique cells, Professor Meshorer and Ph.D. student Alva Biran from Hebrew University collaborated with Dr. Paula Scaffidi and Dr. Christina Morales Torres from the London Creek Institute. The international research team also includes Dr. Ayelet Hashahar Cohen from Hebrew University, Dr. Rotem Ben-Hamo and Professor Sol Efroni from Bar-Ilan University, and Dr. Tom Misteli from the NIH National Cancer Institute.
The team found that among many cancer types, those cancer stem cells lost one of their DNA packaging proteins, H1.0. The H1.0 gene is expressed by binding to DNA.
Professor Meshorer explained: "We found that the disappearance of H1.0 is crucial for cancer cells to remain active. To understand the mechanism of action, we mapped the interaction with DNA and found that it binds to the regulatory region of the gene, when H1 With elevated levels of .0, these genes are able to inhibit the spread of cancer cells."
This research is based on epigenetics - a scientific field that investigates the expression of DNA by switching genes on and off. To identify cancer stem cells from other cells in the tumor, the team studied the epigenetic mechanisms that distinguish the least sorted cells, with unlimited cleavage properties and potential for growth, and more sorted cells lacking this ability. .
The results show an inverse relationship between H1.0 and cancer cell division: as H1.0 levels decrease, the potential for uncontrolled cell division is greater. Conversely, high levels of protein prevent this process, and we find protein H1 The disappearance of .0 is characteristic of cancer stem cells and it is necessary to maintain the ability to divide and the potential for growth.
This discovery opens the door to medical interventions for cancer stem cells, with the goal of restoring high levels of H1.0 in all cancer cells and blocking the differentiation of cancer cells. Although further research is needed to understand the effectiveness of H1.0 protein in preventing cancer growth and spread, this study significantly expressed the mechanisms of cancer stem cells and relatively new epigenetic methods for cancer research.
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