According to a study at the University of North Carolina at Chapel Hill School of Medicine, a new form of protein group is formed that turns the genes "off" and these genes are also found in cancers, reports Medical Xpress.
The study links a form of proteins called polycomb-like proteins, or PCL's, as connecting molecules between the "on" and "off" state of a gene, according to Medical Xpress. The unique type of cells share similar genetic information that is encoded in our DNA. It's understandable that epigenetics, the information outside the genome, that is essential in arranging the reprogramming of a stem cell down the definite path.
"This finding has important implications for both stem cell biology and cancer development, as the same regulatory circuits controlled by PCL's in stem cells are often misregulated in tumors," said Dr. Greg Wang, senior author of the study and Assistant Professor of Biochemistry and Biophysics in the UNC School of Medicine and a member of UNC Lineberger Comprehensive Cancer Center, according to Medical Xpress.
The study shows that a group of proteins called PRC2 complex, which turns the genes off are generated when the PCL's connect with an epigenetic signal that is associated with the genes that recruits PRC2. This study is led by postdoctoral research fellows Drs. Ling Cai and Rui Lu in the Wang lab, and Dr. Scott Rothbart, a Lineberger postdoctoral fellow in the lab of Dr. Brian Strahl, Associate Professor of Biochemistry and Biophysics in the UNC School of Medicine and a member of UNC Lineberger Comprehensive Cancer Center.
"In stem cells, the PRC2 complex turns genes off that would otherwise promote reprogramming into specialized cells of organs like the heart or lungs," said Wang. Wang and his team is focused to develop a drug which can target PRC2 to function in a controlled fashion. "The identification of a specific PCL in controlling PRC2 in cancer cells suggests we may be able to develop drugs targeting this PCL to regulate PRC2 function in a more controlled manner that may maintain PRC2 function in stem cells while inhibiting it in the tumor."
This study is published in the journal Molecular Cell.
