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A Srug Molecule Suggests New Cancer-Treatment Options

Nov, 2021

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A team of researchers from the University of Southern California and the University of North Carolina introduced a new drug-like molecule that can block the effects of mutant epigenetic regulators, which are expected to induce some cancer types, such as lymphoma.

Epigenetic regulators play an important function in healthy cells, turning on and off the activities of multiple genes in the perfectly organized sequence that drives regular human development. A few of these epigenetic regulators, EZH2, regulate the transitory inactivation of particular genes to allow immune cells to mature. Furthermore, a mutant EZH2 gene may induce prolonged suppression of these genes, prohibiting immune cells from growing normally and eventually transforming them into malignant tumors. The best part is that, unlike many other mutations that occur, cancer-causing epigenetic regulator alterations may be reversible with therapeutic medications.

With this in mind, the research group set out to create a drug-like molecule that would reverse EZH2's cancer-causing gene suppression. The researchers began by investigating the method through which EZH2 regulates gene repression. EZH2 works as a writer, indicating which genes will be suppressed. CBX8, a second epigenetic regulator, acts as a reader that reads these repressive marks and activates increased regulatory machinery to turn the genes off. In comparison to the writer, the reader CBX8 appears to be equally important for cancer cell proliferation but less important for healthy cell function.

This indicates that medications aimed against the reader should have fewer damaging symptoms on a patient's healthy cells around the body. To target specific CBX8, the researchers first created mouse stem cells that allowed them to efficiently screen a huge number of drug-like molecules. CBX8 read the marks imprinted by EZH2 to inhibit a gene that produces a detectable green fluorescent protein in these modified stem cells. If the stem cells activated the recognizable green light, the researchers knew that a drug-like molecule had successfully stopped CBX8 from detecting the repressive markings.

The researchers then applied their understanding of CBX8 to many iterations of drug-like compounds aimed at this specific reader. They considered CBX's complicated protein structure and also how it attaches to DNA and reads repressive tags. They proceeded on to experiment in human cancer cells after successfully manufacturing a powerful chemical that functioned well in modified mice cells.

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