Final answer:
Cyclin-dependent kinases can prevent apoptosis by promoting anti-apoptotic genes. The resistance of cancer cells to apoptosis can be due to mutations, loss of receptors, or overexpression of growth factor pathways. The p53 protein plays a key role in regulating apoptosis in response to cell cycle anomalies.
Step-by-step explanation:
Proteins such as cyclin-dependent kinases (Cdks) can stop apoptosis by inducing the expression of anti-apoptotic genes. When exploring why cancer cells might not die after being exposed to an apoptosis inducer, several hypotheses could explain their resistance.
Firstly, the cancer cells might have a mutation preventing the initiation of apoptosis signaling. Secondly, the cells could have lost expression of the receptor needed for the apoptosis-inducing ligand. Thirdly, the cancer cells might overexpress a growth factor pathway that inhibits apoptosis. All these possibilities indicate disruptions in normal cell signaling pathways that can lead to unregulated cell growth, most commonly observed in cancerous cells.
The protein p53 is a crucial negative regulatory molecule that can trigger apoptosis if vital cell cycle events do not occur, acting as a tumor suppressor by either halting cell division to allow DNA repair or initiating apoptosis if repairs are not possible. Furthermore, immune cells like cytotoxic T cells and NK cells can induce apoptosis in target cells through the fas ligand molecule, which is a mechanism used by the body to eliminate abnormal or unhealthy cells.