Friday, May 26, 2017
Cells grow and divide during the cell cycle
Cancer is an extremely complex disease, but its definition is quite simple: the abnormal and uncontrollable growth of cells. Researchers from the University of Rochester’s Center for RNA Biology have identified a new way to potentially slow the fast-growing cells that characterize all types of cancer. The findings, reported today in the journal Science and funded by the National Institutes of Health, were made in kidney and cervical cancer cells in the laboratory and are a long way from being applied in people. But, they could be the basis of a treatment option in the future, the authors said.
Cancer: The Cell Cycle Gone Wrong
All cells go through the “cell cycle,” a series of events that culminate in orderly cell growth and division. In cancer, the cell cycle is out of whack; cells divide without stopping and invade surrounding tissues.
Lynne Maquat, Ph.D.
Researchers identified a protein called Tudor-SN that is important in the “preparatory” phase of the cell cycle – the period when the cell gets ready to divide. When scientists eliminated this protein from cells, using the gene editing technology CRISPR-Cas9, cells took longer to gear up for division. The loss of Tudor-SN slowed the cell cycle.
“We know that Tudor-SN is more abundant in cancer cells than healthy cells, and our study suggests that targeting this protein could inhibit fast-growing cancer cells,” said Reyad A. Elbarbary, Ph.D., lead study author and research assistant professor in the Center for RNA Biology and the department of Biochemistry and Biophysics at the University of Rochester School of Medicine and Dentistry.
Elbarbary, who works in the laboratory of senior study author Lynne E. Maquat, Ph.D., a world-renowned expert in RNA biology, adds that there are existing compounds that block Tudor-SN that could be good candidates for a possible therapy.
Putting the Brakes on Cell Growth
Maquat’s team discovered that Tudor-SN influences the cell cycle by controlling microRNAs, molecules that fine tune the expression of thousands of human genes.
When Tudor-SN is removed from human cells, the levels of dozens of microRNAs go up. Boosting the presence of microRNAs puts the brakes on genes that encourage cell growth. With these genes in the “off” position, the cell moves more slowly from the preparatory phase to the cell division phase.
“Because cancer cells have a faulty cell cycle, pursuing factors involved in the cell cycle is a promising avenue for cancer treatment,” noted Maquat, director of the Center for RNA Biology and the J. Lowell Orbison Endowed Chair and professor of Biochemistry and Biophysics.
Maquat, who also holds an appointment in the Wilmot Cancer Institute, and Elbarbary have filed a patent application for methods targeting Tudor-SN for the treatment and prevention of cancer. Research next steps include understanding how Tudor-SN works in concert with other molecules and proteins so that scientists can identify the most appropriate drugs to target it.
Keita Miyoshi, Ph.D., staff scientist in Maquat’s lab, served as lead study author with Elbarbary. Jason R. Myers and John M. Ashton, Ph.D. from the UR Genomics Research Center played an instrumental role in the study analysis.
Read More: Study: A New Way to Slow Cancer Cell Growth
BMB, BSCB Students Win 2017 Edward Peck Curtis Award for Excellence in Teaching by a Graduate Student
Saturday, April 1, 2017
BMB and BSCB graduate students, Lauren Benoodt, Tyler Couch, and Lisa Houston have been selected as joint winners of the 2017 Edward Peck Curtis Award for Excellence in Teaching by a Graduate Student. The students will be presented with a certificate, as well as checks of $700 for each. The three of them were TA’s for IND 408 (Advanced Biochemistry) in the Fall of 2016.
The Edward Peck Curtis Award for Excellence in Teaching by a Graduate Student was established to recognize graduate students who advance the teaching mission of the University by providing highly skilled and innovative undergraduate instruction.
The strongest nominations show innovation in teaching and a positive impact on the learning of undergraduates.
Congratulations Lauren, Tyler, and Lisa!
Tuesday, February 7, 2017
Lynne E. Maquat, Ph.D. has spent her career unraveling what happens in our cells during disease, making seminal contributions to our understanding of RNA’s role in sickness and in health. She’s also committed countless hours to mentoring the next generation of researchers and advocating for young women in the sciences. For these exceptional efforts, she’s receiving the 2017 Lifetime Achievement Award in Science from the international RNA Society.
The J. Lowell Orbison Endowed Chair and Professor in the Department of Biochemistry and Biophysics at the University of Rochester School of Medicine and Dentistry, Maquat began her professional career studying inherited anemias. She discovered a quality control process that blocks the creation of toxic proteins that cause disease. Known as nonsense-mediated mRNA decay or NMD, this process plays a part in one third of all inherited diseases, such as cystic fibrosis and muscular dystrophy, and one third of all acquired diseases, including a number of cancers.
“This award recognizes Lynne’s pioneering contributions to understanding the mechanisms of RNA, as well as her outstanding leadership, support and commitment to our field, including her role as a model for new generations of scientists,” said Juan Valcarcel Juarez, current president of the RNA Society, who works at the Centre for Genomic Regulation in Barcelona, Spain.
James McSwiggen, CEO of the RNA Society, added, “I can’t imagine a more appropriate choice of awardee.”Read More: Maquat Receives Lifetime Achievement Award in Science from International RNA Society