Stem cells reprogram along defined routes to develop molecular mechanisms that form specific organs such as the heart, lungs, or kidneys, and have long been the focus of scientists' research. Researchers from the University of North Carolina at Chapel Hill School of Medicine recently revealed in a new study the mechanism by which epigenetic signals synergistically determine the ultimate fate of stem cells. Related papers were published in the December 27th "Molecular Cell" (Molecular Cell) magazine.

Although the genetic information encoded in the DNA of all specialized cell types is the same, it is becoming increasingly clear that information outside the genome, namely epigenetics, plays an important role in orchestrating the reprogramming of stem cells towards a defined route. Although it is known that epigenetics is the cause of specific genes during cell development that cause genes to turn on and off, the exact mechanism for regulating this delicate process is currently not well understood.

In the new study, the researchers discovered that a unique class of proteins called PCLs (polycomb-like proteins) act as a bridge molecule between the "switch" states of the gene.

Dr. Greg Wang, a senior author of the paper, an assistant professor of biochemistry and biophysics at the University of North Carolina School of Medicine, and a member of the Lineberger Comprehensive Cancer Center, said: "This discovery has important implications for stem cell biology and cancer formation because of the The same regulatory circuits controlled by PCLs often also misregulate in tumors. "

Recent studies have revealed that the two core protein complexes of PRC1 and PRC2 are involved in the establishment and maintenance of the polycomb (Polycomb) inhibition of chromatin state, which is the basis for determining the activation and deactivation of genes and the appropriate cell type at the appropriate time. One of the elements. Among them, PRC2 mediates the methylation regulation of H3K27, which is very important for Polycomb (Pc) gene silencing, which is also a classic epigenetic phenomenon that maintains transcriptional silencing through cell division.

In this new article, the researchers found that PCLs through the PRC2 complex caused certain genes related to epigenetic signals to be turned off.

Greg Wang said: "In stem cells, the PRC2 complex turns off some genes that can promote reprogramming to form specialized cells such as the heart or lungs."

In addition to playing an important role in cell development, increased levels of PRC2 have also been found in various cancer types such as prostate cancer, breast cancer, lung cancer, and blood cancer. Many pharmaceutical companies are starting to develop drugs that target PRC2. Greg Wang and colleagues confirmed that the mechanisms that control the function of PRC2 in stem cells also apply to human cancer.

"A specific PCL that can control PRC2 is found in cancer cells. We may be able to develop a drug that targets this PCL to regulate PRC2 function in a more controlled manner to maintain the function of PRC2 in stem cells and in tumors. Suppress it, "Greg Wang said.

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