Final answer:
Survival factors can induce the anti-apoptotic gene through proteins like p53. If cells do not die when apoptosis is induced, it could be due to mutations that prevent apoptosis initiation, lack of apoptosis receptor expression, or overexpression of inhibitory growth factor pathways. Mutations in p53 can lead to uncontrolled cell growth and cancer.
Step-by-step explanation:
Survival factors can induce the expression of the anti-apoptotic gene when cells experience cellular stress or DNA damage. These factors often prevent programmed cell death (apoptosis) by activating specific pathways or genes.
One well-known protein associated with such regulation is p53, which plays several roles, including the arrest of the cell cycle to allow for DNA repair, or the initiation of apoptosis when repair is not possible. It is a key tumor suppressor and can induce anti-apoptotic genes or halt cell proliferation.
When a scientist notices that a cancer cell line fails to die after adding an inducer of apoptosis, there could be several reasons for this observation.
The cells might have a mutation preventing the initiation of apoptosis signaling, they could have lost expression of the receptor for the apoptosis-inducing ligand, or the cells might overexpress a growth factor pathway that inhibits apoptosis. The correct hypothesis that explains why the cells fail to die is d. All of the above.
Each of these reasons can contribute to the resistance of cells to apoptosis, which is common in cancerous cells.
Moreover, mutated p53 genes are found in over half of all human tumor cells, which emphasizes the crucial role this protein plays in preventing the proliferation of damaged cells.
A functional p53 protein can halt the cell cycle, initiate DNA repair, or trigger apoptosis to prevent the spread of mutations. In contrast, mutations of the p53 gene result in an inability to control cell proliferation and apoptosis, often leading to cancer.