Final answer:
The statement is false as Myc is an oncogene that promotes tumor growth and Bcl-2 and Bcl-xL are anti-apoptotic proteins, not proto-oncoproteins. Proto-oncogenes, when mutated, can become oncogenes leading to uncontrolled cell growth.
Step-by-step explanation:
The statement provided is false: Pro-survival proteins such as Myc do not synergize with proto-oncoproteins like Bcl-2, Bcl-xL to enhance tumorigenesis because Myc is itself an oncogene when overexpressed and Bcl-2 and Bcl-xL are anti-apoptotic proteins that can contribute to cancer development by preventing programmed cell death. Proto-oncogenes are indeed positive cell-cycle regulators that, when mutated or overexpressed, can become oncogenes which lead to uncontrolled cell growth and cancer. Myc is a transcription factor that can be aberrantly activated in cancers such as Burkitt's Lymphoma, causing uncontrolled growth of B cells, which can form tumors. On the other hand, tumor suppressor genes encode proteins that block cell cycle progression and promote apoptosis, acting as the cell's 'brakes' in contrast to the 'accelerator' function of oncogenes.