The cell cycle is a series of events that a cell goes through as it grows and divides. The decision of whether or not to divide is made at a critical point in the cell cycle called the G1/S checkpoint. If the cell has enough nutrients and growth factors, it will proceed to the S phase of the cell cycle and begin to replicate its DNA. However, if the cell is stressed or lacks the necessary resources, it will arrest at the G1/S checkpoint and will not divide.
In the new study, the UCSF researchers found that cells can reverse their decision to arrest at the G1/S checkpoint and proceed to divide. This happens when the cells are exposed to a growth factor called insulin-like growth factor 1 (IGF-1). IGF-1 activates a signaling pathway that leads to the phosphorylation of a protein called Rb. Phosphorylated Rb releases a transcription factor called E2F, which promotes cell cycle progression.
The researchers also found that the ability of cells to reverse their decision to arrest at the G1/S checkpoint is controlled by a microRNA called miR-21. miR-21 is a small RNA molecule that regulates gene expression. The researchers found that miR-21 levels are increased in cells that are exposed to IGF-1, and that miR-21 is necessary for the cells to reverse their decision to arrest at the G1/S checkpoint.
The new study provides insights into how cells make the decision to divide and how this decision can be reversed. This knowledge could have implications for understanding and treating cancer, as well as for developing new regenerative therapies. For example, the researchers suggest that it may be possible to use IGF-1 or miR-21 to promote the growth of new tissue in patients who have suffered from a stroke or heart attack.
The study was published in the journal Nature Cell Biology.
