Final answer:
Alterations in proteins that inhibit or promote apoptosis, as well as proteins that regulate the cell cycle checkpoints, can cause a cell to proliferate more than it should, potentially leading to cancer. The p53 protein and cyclins are key examples of such regulatory proteins.
Step-by-step explanation:
The alterations that could cause a cell to proliferate more than it should include alteration of a protein that normally inhibits apoptosis, alteration of a protein that normally promotes apoptosis, and alteration of a protein that normally prevents process through the cell cycle if there is something wrong.
Apoptosis is the programmed cell death that is a crucial process in maintaining healthy tissue homeostasis. Proteins that inhibit apoptosis can, when altered, prevent cells from undergoing programmed cell death even when they are faulty, leading to unchecked cell proliferation. On the other hand, proteins that promote apoptosis, when altered, might also lead to reduced cell death and increased cell survival. Proteins responsible for checkpoint controls in the cell cycle play an important role in detecting and repairing damaged DNA. If these proteins are altered, cells with DNA damage might continue to divide, leading to potential cancer development.
The p53 protein is an example of a molecule that acts at a cell cycle checkpoint to detect DNA damage and initiate repair or apoptosis. A mutated p53 cannot trigger cell death, allowing damaged cells to proliferate, which is often observed in cancer cells. Cyclin proteins, which regulate the cell cycle progression, when mutated, can also lead to abnormal cell proliferation and potentially cancer.
Overall, in the case of cancer cell lines, they may fail to die upon induction of apoptosisdue to mutations that prevent initiation of apoptosis signaling, loss of receptor expression for the apoptos is-inducing ligand, or the overexpression of growth factor pathways that inhibit apoptosis.