促癌蛋白,抑癌基因 z-bo 2020-08-17 569

　　Researchers at the University of California, San Diego School of Medicine have discovered that proteins necessary to regulate cell cycle progression (the process of cell division and replication) actually activate important tumor suppressor genes, not previously thought.

　　"This discovery is the result of 20 years of research in my laboratory," said Dr. Stephen F. Daudi, professor of cell and molecule at the University of California San Diego School of Medicine. "This completely overturns the traditional concept that the most common genetic pathway mutation in cancer is called the p16-cyclin D pathway, which promotes the basic aspects of the cell cycle progression of all tumor cells." Published in "eLife" magazine. Cyclin D is synthesized in the initial stage of cell replication and is believed to help promote a complex multi-step process involving interaction with retinoblastoma (Rb) protein and Rb protein. Its function is to inhibit cell cycle progression. Until the cell is ready to divide to prevent cell overgrowth. B is a tumor suppressor gene. Several major Rb mutations and dysfunctions associated with cancer and cyclin D are thought to inhibit Rb through a process called phosphorylation, and therefore are described as cancer-promoting oncogenes. Function failure.

　　Daodi and his colleagues carefully calculated the amount of phosphate added to Rb during the cell cycle. There are as many as 14 kinds, but scientists found that cyclin D only adds one kind of phosphoric acid. In the early G1 stage of the cell cycle, only one of 14 sites, basically 14 different subsites of Rb. I found that there is a type. The role of monophosphate is to activate RB without inactivating it, and this knowledge has existed for more than 20 years. The researchers said that this study has fundamentally changed people's understanding of the G1 cell cycle regulation and the origin of many cancer-related molecules.

　　It is important to understand the actual function of gene pathways and the consequences of their destruction, especially when multiple cyclin D inhibitors are used in breast cancer clinical trials.