Final answer:
In human cell lines, oncogenic transformation can be achieved with SV40 T antigen, ras-V12, and hTERT (telomerase). The large T antigen of SV40 affects p53 function, allowing for uncontrolled cell division, while hTERT maintains telomere length, enabling cells to divide indefinitely, which is a characteristic of cancer cells.
Step-by-step explanation:
In human cell lines, normal tissue types can be transformed to oncogenic lines by the introduction of SV40 T antigen, ras-V12, and hTERT (telomerase). The stated elements are instrumental in the transformation process. SV40 T antigen interacts with p53, compromising its function and leading to uncontrolled division.
Viral-oncogenes (v-onc), present in acutely transforming viruses, can directly transform cells immediately upon expression. In contrast, in slowly-transforming viruses, overexpression of proto-oncogenes occurs due to viral genome insertion, which leads to uncontrolled cellular proliferation over time.
Specifically, the introduction of hTERT, which is the catalytic subunit of the enzyme telomerase, relates to maintaining telomere length, an essential feature for the immortalization of many cancer cell lines like HeLa cells.
This is because telomerase activity counters the usual shortening of telomeres with each cell division, thus permitting cells to bypass the senescence and continue dividing indefinitely, a hallmark of many cancers. Interestingly, hTERT has been found necessary for the rapid proliferation of cells in human embryos as well.
It should be noted that factors like laminin, Cdc13, TRF2, and SIR3/SIR4 play roles in different cellular contexts but are not typically key players in the direct transformation of normal human tissue into an oncogenic line in the same way SV40 T antigen, ras-V12, and hTERT are.