Oncogenes carry the genetic blueprint for proteins that cause unregulated cell proliferation. However, these proteins usually need to interact with other partners in order to trigger the tumour growth. If this interaction is disturbed, the tumour stops growing.
Scientists at the universities of Würzburg and Stanford – among them Martin Eilers –now have succeeded for the first time in confirming this theory with examinations performed on a living organism.
Nearly all human cells have a certain group of genes, which play an important role in the formation of cancer – the so-called Myc genes. Usually these genes are not read out frequently; they serve as a blueprint for Myc proteins, which fulfil some functions in cell growth and are required only in small amounts.
If the Myc genes do not work properly, the cells start to divide, resulting in tumour formation. "The theory that Myc proteins bind to another protein, the Miz1 protein, to regulate a group of genes important for tumour growth has already been in place since 1997," explains Eilers. "Tumour cells cannot do without the continuous support from the genes responsible for their formation. If this support is lacking, the tumour cell collapses. Until now the reasons for this have never been fully understood," he adds. The phenomenon can be explained by the Myc-Miz interaction.
"Tumour cells carry an intracellular program, the actual function of which is to prevent them from proliferating without control," explains Eilers. In other words: A tumour cell tends to commit suicide or to refuse to work. Firstly, it can start the process of programmed cell death – a damaged cell kills itself off to protect the organism from greater harm (apoptosis). Secondly, the cell can stop to divide but still remains physiologically active (senescence).
The senescence is only prevented via the interaction with the Miz1 protein. The scientists were able to prove this by modifying the Myc gene at a specific location. As a consequence, the corresponding protein was altered in such a way that it could no longer bind effectively to Miz1.
So far, the findings have no direct consequences for cancer therapy.
MEDICA.de; Source: Julius-Maximilians-Universität Würzburg