Cell division is a critical process in the human body, with only about 30 minutes spent on mitosis, where chromosomes are distributed to daughter cells. However, if this process takes too long, it can lead to damaged and diseased cells that may progress to cancer. Researchers at the University of California San Diego have identified a key mechanism that monitors the timing of mitosis and detects when it is prolonged. This mechanism acts as a “stopwatch” that prevents problematic cells from further proliferating.
The stopwatch mechanism is part of a biochemical pathway that constantly monitors the time spent in mitosis and accumulates delays from one cell generation to the next. The pathway involves three proteins, including p53, which is commonly mutated in human cancers. Through experiments, researchers observed that even a delay of as little as 20 minutes in cell division is considered risky. This quality control mechanism ensures that cells with prolonged mitosis are stopped from dividing further as a safety measure.
The researchers believe that the 30 minutes allocated for mitosis may have evolved as a way to quickly navigate through a crucial but potentially hazardous phase of cell division. Cancers are viewed as foreign entities within the body, and the stopwatch mechanism acts as a surveillance system to detect and eliminate problematic cells. Interestingly, many types of cancers deactivate this mechanism, allowing them to tolerate abnormal genomes that experience extended and problematic mitoses. This research suggests that measuring mitosis time is a protective mechanism developed to defend against cellular abnormalities.
In the future, the findings of this study could have implications for cancer treatment strategies. The researchers propose that the status of the stopwatch mechanism could influence the effectiveness of therapeutic agents targeting mitotic processes. This mechanism could potentially serve as a biomarker to guide the use of specific cancer treatments. The discovery of the stopwatch mechanism sheds light on another tumor-suppression function associated with p53’s role in protecting against abnormal cells.
The study’s coauthors, Franz Meitinger, Hazrat Belal, Robert Davis, Mallory Martinez, Andrew Shiau, Karen Oegema, and Arshad Desai, have provided valuable insights into the regulation of mitosis timing and cell division. By understanding how cells monitor and respond to delays in mitosis, researchers may be able to develop more targeted and effective treatments for cancer patients. The discovery of this stopwatch mechanism opens up new avenues for exploring novel approaches to cancer therapy based on mitotic processes and cellular surveillance mechanisms.
