Final answer:
Increased p21, regulated by p53, inhibits Cdk/cyclin complexes at the G1 checkpoint, halting cell cycle progression when DNA damage is detected. If p53 is mutated and cannot induce p21, the checkpoint is compromised, allowing potentially damaged cells to divide and promoting tumor growth.
Step-by-step explanation:
Increased levels of p21 function as a key regulator in blocking the cell cycle, primarily at the G1 checkpoint. The protein p53 plays a crucial role when there is damaged DNA in a cell preparing for division during G1. Upon detecting DNA damage, p53 acts to halt the cycle and initiates repair mechanisms. If repair is not possible, p53 can trigger apoptosis to prevent the propagation of damaged DNA.
When p53 function is lost due to mutation, it may fail to activate p21 production, removing the effective block on Cdk activation. Without this block, the G1 checkpoint cannot properly function, allowing the cell to proceed from G1 to S phase regardless of DNA damage, leading to potential tumor growth as mutated and damaged cells replicate.