Final answer:
Procaspase 8 dimers have the function of activating apoptosis, a process of programmed cell death crucial for eliminating damaged cells. Resistance to apoptosis in cancer might involve mutations blocking apoptotic signaling, receptor loss, or overactive growth factor pathways. Tumor suppressor genes ensure cell integrity by preventing the division of cells with damaged DNA and can induce apoptosis if repair is not possible.
Step-by-step explanation:
The function of procaspase 8 dimers is to activate apoptosis. Apoptosis is a form of programmed cell death that is essential for the removal of damaged or unnecessary cells. When activated, procaspase 8 forms part of the death-inducing signaling complex (DISC) that triggers a cascade of events leading to cellular breakdown. The activation involves cleaving procaspase 8 into smaller active caspases, which then cleave other target proteins to execute the apoptotic process.
Regarding possible hypotheses why a cancer cell line may not undergo apoptosis upon induction, several factors could play a role, including: a mutation that inhibits the initiation of apoptosis signaling, loss of expression of the apoptosis-inducing receptor, or the overexpression of a growth factor pathway that inhibits apoptosis. All of the above could contribute to the cancer cells' resistance to the programmed cell death.
Tumor suppressor genes play a critical role in regulating the cell cycle and preventing cancer growth. Their primary function is to stop certain cells from dividing, especially when there are abnormalities such as damaged DNA. The tumor suppressor p53 is particularly important, as it can halt the cell cycle to allow DNA repair or, if the damage is irreparable, initiate apoptosis to prevent the propagation of flawed genetic material.