Subverting traditional cognition, cancer-promoting proteins actually activate tumor suppressor genes

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

  "This discovery is the result of 20 years of research in my laboratory," said Dr. Stephen F. Daudi, professor of cell molecules 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." The research results are published in the "eLife" magazine Published. Cyclin D is synthesized in the first step of cell replication and is believed to help facilitate complex multi-step processes, including interaction with retinoblastoma (Rb) protein, Rb protein. Prevent cell overgrowth by inhibiting cell cycle progression until the cell is ready to divide. B is a tumor suppressor gene. Several major Rb mutations and dysfunctions associated with cancer and cyclin D have been described as cancer-promoting genes because they are thought to inhibit Rb through a process called phosphorylation. Function failure.

  Daodi and his colleagues carefully calculated the amount of phosphate added to Rb during the cell cycle. There are about 14 of them, but it was found that cyclin D has only one additional monophosphate, which is only one of the 14 sites in the G1 phase of the early cell cycle process. 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 research has fundamentally changed people's understanding of the G1 cell cycle regulation and the origin of many cancer molecules. Understanding the actual function of gene pathways and the consequences of their destruction, especially when using multiple cyclin D inhibitors in breast cancer clinical trials is particularly important.