This makes it a good target for new drugs. BEND3 seems to be a central player in the process of determining the fate of a cell, noted Prasanth. There are other cell cycle regulators, some of which BEND3 interacts with. When BEND3 is removed, the cells move toward differentiation. When BEND3 binds to the cell cycle genes, the cells don't differentiate. They determined that many of those downregulated genes can encourage cells to differentiate. "But what does it really mean?" In this study, the researchers answered that question. "When you do these gene-expression studies, you can see hundreds of genes go up, hundreds down," Prasanth said. If BEND3 was eliminated, that expression was restored. It may be possible to improve cancer treatments by switching malignant cells from a proliferation to differentiation mode A cell cycle regulator may be able to do that.īEND3 is known to be important to the cell cycle, and Prasanth's team determined that it can block or reduce gene expression when it binds to various parts of the genome. If a therapy successfully shrinks a tumor, continued Prasanth, stem cells can repopulate the cells that were ablated, restoring the tumor. The more differentiated a tumor is, the better the prognosis." Supriya Gangadharan Prasanth's 3 research works with 12 citations and 88 reads, including: Expression of Protooncogene c-kit Receptor in Rat Testis and Uniqueness of Extracellular Domain Across. Prasanth added that predictions about how well cancers will respond to treatments are often related "to its status of differentiation. Cells typically stop proliferating actively when they are fully differentiated. In many cancer cells, proliferation is unrestrained, because the checks on the cell cycle are not working as they should, said Prasanth. This research has provided new insights into developmental processes and may also apply to cancer research, said study leader Supriya Prasanth, a department chair and professor at the University of Illinois Urbana-Champaign. Cells specialized and gained their identity only when BEND3 was downregulated. Reporting in the Proceedings of the National Academy of Sciences (PNAS), a molecule called BEND3 was found to turn off hundreds of genes that are linked to differentiation and the maintenance of pluripotency. Researchers have now learned more about how cells turn pluripotency off, and settle into their final functional form. Scientists have been studying those cues and signals for a long time so the process can be understood and controlled. Like embryonic stem cells, pluripotent stem cells can also specialize into any type of cell in the body by following biochemical cues.