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Researchers Discover Protein Function That Could Improve Chemotherapy in the Future

AHA Publisher — Fri, 18 Dec 2020 08:00:01 +0000

University of Copenhagen the Faculty of Health and Medical Sciences via EurekAlert – Chemotherapy attacks all cells in our body and not just cancer cells, which is why patients undergoing the treatment often experience side effects such as physical weakness, hair loss and nausea. However, because cancer cells divide and spread faster than most normal cells, cancer cells are more sensitive to chemotherapy, which kills cells by inhibiting their ability to spread. Chemotherapy often targets and damages DNA so that cancer cells can no longer replicate their genome, which is the process of copying the genetic information, and stop the growth and die. However, cancer cells may find ways to escape the chemotherapy. When attacked by chemotherapy, cells – including cancer cells – will try to repair or bypass the damage. A group of researchers at the Faculty of Health and Medical Sciences, University of Copenhagen, are trying to figure out how cells repair or bypass the lesions induced by chemotherapy, in the hope to provide new methods to inhibit these repair processes and make the chemotherapy more efficient. In a new collaborative work with different laboratories at the Center for Protein Research, Associate Professor Julien Duxin and his group have revealed a protein that seems to play a vital role in recruiting DNA key repair and signaling factors. If they are right, the discovery could be important for future chemotherapy treatment. ‘We have found strong evidence that the protein RFWD3 is responsible for orchestrating the repair of different DNA lesions induced by chemotherapy. If we can inhibit this protein, we could potentially block cells from tolerating DNA lesions, which could lead to more effective chemotherapy in the future’, says Julien Duxin, group leader at The Novo Nordisk Foundation Center for Protein Research. Uncovering the Knowledge Gap The findings, published in Molecular Cell, is the culmination of three years of research at the Duxin Group. The group focuses on understanding the basic principles of DNA replication and DNA repair which allow cells to repair genomic lesions like the ones induced by chemotherapy says Julien Duxin. ‘Since the 1950s and the pioneer work from Sydney Farber, we have been treating cancer patients with different types of chemotherapeutic agents. These are extremely toxic agents, which have been approved in the clinic because they are effective at killing cancer cells. But the truth is that we still don’t know how cells can repair the damage caused by the treatment. It is a huge knowledge gap, which we are trying to fill in with our fundamental research’, he says. Using egg extracts from African frogs, which contain the same repair factors than the ones present in our cells, the group was able to identify the protein RFWD3 as a critical coordinator of the repair events that happen when cells are replicating across from DNA lesions. The group observed that the absence of the protein leads to a profound defect in recruitment of the components needed to repair and tolerate the damage. ‘Repairing DNA lesions is a complex sequence of multiple events. Our goal is to identify the proteins at each event, which are essential to do this type of repair’, says Julien Duxin. Little is known about how repair works across different kinds of DNA damage. The group is now trying to set up simple systems so it becomes possible to molecularly study how these damages are repaired, Julien Duxin explains. ‘We have very little knowledge about how most of these lesions caused by chemotherapy are repaired inside our cells. We are setting up different model systems to study this in detail and identify the key enzymes essential to this process. And by knowing those key enzymes we also get key targets that companies can aim to inhibit’, he says. To read the original article click here.

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Coronavirus Makes Changes That Cause Cells Not to Recognize It

AHA Publisher — Wed, 29 Jul 2020 07:00:04 +0000

North Carolina State University via EurekAlert – With an alarm code, we can enter a building without bells going off. It turns out that the SARS coronavirus 2 (SARS-CoV-2) has the same advantage entering cells. It possesses the code to waltz right in. On July 24 in Nature Communications, researchers at The University of Texas Health Science Center at San Antonio (UT Health San Antonio) reported how the coronavirus achieves this. The scientists resolved the structure of an enzyme called nsp16, which the virus produces and then uses to modify its messenger RNA cap, said Yogesh Gupta, PhD, the study lead author from the Joe R. and Teresa Lozano Long School of Medicine at UT Health San Antonio. “It’s a camouflage,” Dr. Gupta said. “Because of the modifications, which fool the cell, the resulting viral messenger RNA is now considered as part of the cell’s own code and not foreign.” Deciphering the 3D structure of nsp16 paves the way for rational design of antiviral drugs for COVID-19 and other emerging coronavirus infections, Dr. Gupta said. The drugs, new small molecules, would inhibit nsp16 from making the modifications. The immune system would then pounce on the invading virus, recognizing it as foreign. “Yogesh’s work discovered the 3D structure of a key enzyme of the COVID-19 virus required for its replication and found a pocket in it that can be targeted to inhibit that enzyme. This is a fundamental advance in our understanding of the virus,” said study coauthor Robert Hromas, MD, professor and dean of the Long School of Medicine. Dr. Gupta is an assistant professor in the Department of Biochemistry and Structural Biology at UT Health San Antonio and is a member of the university’s Greehey Children’s Cancer Research Institute. In lay terms, messenger RNA can be described as a deliverer of genetic code to worksites that produce proteins. To read the original article click here.

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Device Could ‘Hear’ Disease Through Structures Housing Cells

AHA Publisher — Tue, 24 Mar 2020 07:00:48 +0000

Purdue University via EurekAlert – Similarly to how a picked lock gives away that someone has broken into a building, the stiffening of a structure surrounding cells in the human body can indicate that cancer is invading other tissue. WEST LAFAYETTE, Ind. — Monitoring changes to this structure, called the extracellular matrix, would give researchers another way to study the progression of disease. But detecting changes to the extracellular matrix is hard to do without damaging it. Purdue University engineers have built a device that would allow disease specialists to load an extracellular matrix sample onto a platform and detect its stiffness through sound waves. The device is described in a study published in the journal Lab on a Chip and demonstrated in a YouTube video at https://youtu.be/hPvY0Sj0vxY. “It’s the same concept as checking for damage in an airplane wing. There’s a sound wave propagating through the material and a receiver on the other side. The way that the wave propagates can indicate if there’s any damage or defect without affecting the material itself,” said Rahim Rahimi, a Purdue assistant professor of materials engineering, whose lab develops innovative materials and biomedical devices to address health care challenges. Each tissue and organ has its own unique extracellular matrix, sort of like how buildings on a street vary in structure depending on their purpose. The extracellular matrix also comes with “landlines,” or structural and chemical cues, that support communication between individual cells housed in the matrix. Researchers have tried stretching, compressing or applying chemicals to samples of the extracellular matrix to measure this environment. But these methods also are prone to damaging the extracellular matrix. Rahimi’s team developed a nondestructive way to study how the extracellular matrix responds to disease, toxic substances or therapeutic drugs. The initial work for this study was performed in collaboration with the lab of Sophie Lelièvre, a professor of cancer pharmacology at Purdue, to identify how risk factors affect the extracellular matrix and increase the risk of developing breast cancer. The device is a “lab-on-a-chip” connected to a transmitter and receiver. After pouring the extracellular matrix and the cells it contains onto the platform, the transmitter generates an ultrasonic wave that propagates through the material and then triggers the receiver. The output is an electrical signal indicating the stiffness of the extracellular matrix. The researchers first demonstrated the device as a proof-of-concept with cancer cells contained in hydrogel, which is a material with a consistency similar to an extracellular matrix. The team now is studying the device’s effectiveness on collagen extracellular matrices. The device could easily be scaled up to run many samples at once, Rahimi said, such as in an array. This would allow researchers to look at several different aspects of a disease simultaneously. To read the original article click here.

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Anxiety Disorders Linked to Disturbances in the Cells’ Powerhouses

AHA Publisher — Fri, 04 Oct 2019 07:00:34 +0000

PLOS via News Wise – The discovery that high levels of stress may substantially impact the functioning of the powerhouses of the cell opens up new avenues of research into stress-related diseases. Newswise — The powerhouse of the cell, the mitochondria, provides energy for cellular functions. But those activities can become disturbed when chronic stress leads to anxiety symptoms in mice and humans. Iiris Hovatta of the University of Helsinki and colleagues report these findings in a new study published 26th September in PLOS Genetics. Chronic stress due to stressful life events, such as divorce, unemployment, loss of a loved one and war, are a major risk factor for developing panic attacks and anxiety disorders. Not all people who experience stressful life events go on to develop a disorder, however, and scientists are trying to identify the pathways that lead some people to be resilient to stress, while others become vulnerable to anxiety. In the current study, researchers studied mice that developed symptoms of anxiety and depression, such as avoiding social interactions, after being exposed to high levels of stress. Using a multi-pronged approach, they tracked changes in gene activity and protein production in a key region of the brain for stress-response and anxiety. The analysis pointed to a number of changes in the mitochondria in the brain cells of mice exposed to frequent stress, compared to the non-stressed mice. Furthermore, testing of blood samples collected from patients with panic disorder after a panic attack also showed differences in mitochondrial pathways, suggesting that changes to cellular energy metabolism may be a common way that animals respond to stress. The discovery that high levels of stress may substantially impact the functioning of the powerhouses of the cell opens up new avenues of research into stress-related diseases. “Very little is known about how chronic stress may affect cellular energy metabolism and thereby influence anxiety symptoms,” said author Iiris Hovatta. “The underlying mechanisms may offer a key to new targets for therapeutic interventions of stress-related diseases.” Further studies of what causes these changes to the mitochondria may provide much needed insight into the molecular basis of panic disorder and other anxiety disorders. This is a critical step in developing better therapies to treat anxiety. To read the original article click here.

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