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Putting the brakes on cancer

Cancer is an extremely complex disease, but its definition is quite simple — it is 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 which characterize all types of cancer.


Every cell of the body goes through a "cell cycle," or a series of molecular interactions that end in cell division and, therefore, tissue growth. In cancers, for some reason or reasons, the cell cycle becomes unsynchronized. Cells cannot stop dividing and eventually begin invading and disrupting surrounding tissues.

University of Rochester Medical researchers now have identified one protein, Tudor-SN, critically important to the "preparatory" phase of a normal cell cycle. The preparatory phase signals a cell to get ready to divide. However, when scientists cut out the Tudor-SN protein using gene editing technology called CRISPR-Cas9, that cell took longer to get to division. So, increasing the amount of microRNAs put the "brakes" on genes — turning them “off”.

These findings, reported in the journal Science and funded by the National Institutes of Health, were made in kidney and cervical cancer cells.


"We know that Tudor-SN is more abundant in cancer cells than in healthy cells. Our study suggests that targeting this protein could inhibit fast-growing cancer cells."

Reyad A. Elbarbary PhD, Assistant Professor, Center for RNA Biology, Department of Biochemistry and Biophysics, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA.


Elbarbary works in the laboratory of Lynne E. Maquat PhD, a world-renowned expert in RNA biology. Maquat knows there are existing compounds that block Tudor-SN which could be good candidates for a possible medicinal therapy. Her team's discovery of how Tudor-SN influences the cell cycle by controlling microRNAs, molecules known to fine tune the function of thousands of human genes, has the potential to impact many if not all cancer treatments.

When Tudor-SN is removed from human cells, the amount of dozens of microRNAs increases. Boosting microRNAs puts the brakes on genes that encourage cell division/growth, turning them "off". Now, the cell moves more slowly from the preparatory phase to division phase.

"Because cancer cells have a faulty cell cycle, pursuing factors involved in the cell cycle is a promising avenue for cancer treatment."

Lynne E. Maquat PhD, Professor of Biochemistry and Biophysics, and Director, Center for RNA Biology, and holder of the J. Lowell Orbison Endowed Chair.


Maquat, who also holds an appointment in the Wilmot Cancer Institute, will pursue along with Elbarbary, a patent application for methods targeting Tudor-SN for treatment and prevention of cancer. Their research next steps include determining how Tudor-SN interacts with other molecules and proteins to identify the most effective combinations for its elimination.

Breaking down miRNAs
Although much work has examined microRNA (miRNA) biogenesis, relatively little is known about miRNA decay. Elbarbary et al. now identify Tudor-SN, an endonuclease that interacts with the RNA-induced silencing complex. Tudor-SN targets miRNAs at CA and UA dinucleotides located more than five nucleotides from miRNA ends. Tudor-SN-mediated miRNA decay removes miRNAs that silence genes encoding proteins that are critical for the G1-to-S phase transition in the cell cycle.

Abstract
MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression. The pathways that mediate mature miRNA decay are less well understood than those that mediate miRNA biogenesis. We found that functional miRNAs are degraded in human cells by the endonuclease Tudor-SN (TSN). In vitro, recombinant TSN initiated the decay of both protein-free and Argonaute 2–loaded miRNAs via endonucleolytic cleavage at CA and UA dinucleotides, preferentially at scissile bonds located more than five nucleotides away from miRNA ends. Cellular targets of TSN-mediated decay defined using microRNA sequencing followed this rule. Inhibiting TSN-mediated miRNA decay by CRISPR-Cas9 knockout of TSN inhibited cell cycle progression by up-regulating a cohort of miRNAs that down-regulates mRNAs that encode proteins critical for the G1-to-S phase transition. Our study indicates that targeting TSN nuclease activity could inhibit pathological cell proliferation.

Other authors: Keita Miyoshi PhD 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.


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May 24, 2017   Fetal Timeline   Maternal Timeline   News   News Archive   

blood stem and progenitor cells

All cells go through a "cell cycle," which is a series of molecular events that promote cell growth through division. In cancer, this cell cycle is out of synch. Cells divide uncontrollably and invade surrounding tissues. By removing a specific protein from cells, researchers were able to slow the
cell cycle. The findings were made in kidney and cervical cancer cells and are a long way from
being applied in people. But, the study suggests targeting this protein could inhibit fast-growing
cancer cells and be the basis of a treatment options in the future.
Image Credit: University of Rochester Medical Center

 


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