Forum for Science, Industry and Business

Sponsored by:     3M 
Search our Site:

 

Cancer: No Tumor without Cooperation

15.06.2010
Tumors disappear if you inhibit the genes responsible for their formation. Previously, any suggestions as to why they behave in this way were nothing more than theories. Researchers at the University of Würzburg now present concrete evidence, confirming a long-held assumption in this matter.

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 tumor growth. If this interaction is disturbed, the tumor stops growing.

Concerning the reasons for this, there has been a theory around for many years, supported by some test-tube findings. Scientists at the universities of Würzburg and Stanford now have succeeded for the first time in confirming this theory with examinations performed on a living organism. Their results are published in the current issue of the scientific journal Genes & Development.

The role of the oncogenes

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 very frequently; they serve as a blueprint for Myc proteins, which fulfill 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 in an uncontrolled way, resulting in tumor formation. The above-mentioned team of scientists have taken a closer look at this process. "The theory that Myc proteins bind to another protein, the Miz1 protein, to regulate a group of genes important for tumor growth has already been in place since 1997," explains Martin Eilers.

Eilers is head of the Department for Physiological Chemistry II at the Biocenter of the University of Würzburg. As early as in 1988, when he conducted his postdoctoral research in San Francisco, he started to study the Myc genes and proteins. He was a member of the research team that developed the theory of the protein interaction in 1997.

Now two of the postgraduate students in his team, Judith Müller and Tobias Otto, together with their colleagues from Stanford University (California), have succeeded in confirming this theory with examinations performed on a living organism.

A genetic mutation reduces the number of cancer diseases

"Tumor cells cannot do without the continuous support from the genes responsible for their formation," says Eilers. If this support is lacking, the tumor 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.

"Tumor cells carry an intracellular program, the actual function of which is to prevent them from proliferating without control," explains Martin Eilers. In other words: A tumor 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 whole organism from greater harm. Scientists refer to this process as apoptosis. Secondly, the cell can stop its life cycle; in this case, it does no longer divide but still remains physiologically active. The technical term for this is cellular 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. In laboratory animals carrying the mutated gene, the cancer rates were significantly reduced. The result is a bit strange: A mutated gene reduces the number of tumors. Isn't it the gene mutations that are usually responsible for a multitude of cancer diseases?

Protein interaction required

So why isn't this true in this case? "Myc needs to bind to Miz1 in order to prevent the cell from producing certain tumor-inhibiting factors," explains Martin Eilers. Myc and Miz cannot impose continuous growth on the cell unless they work together. Only their interaction can prevent the cell from implementing its normal biological aging program.

So far, the findings of the Würzburg and Stanford scientists have no direct consequences for cancer therapy. At present, the Myc-Miz complex does not represent a promising starting point – the process is too complicated for this. "We still do not know enough about its physiological function," says Eilers. Therefore, as a next step, Eilers and his team would like to clarify the role of the protein interaction in the normal development of the cell.

The interaction between Myc and Miz1 is required to antagonize TGFb-dependent autocrine signaling during lymphoma formation and maintenance. Jan van Riggelen, Judith Müller, Tobias Otto, Vincent Beuger, Alper Yetil, Peter S. Choi, Christian Kosan, Tarik Möröy, Dean W. Felsher and Martin Eilers. Genes & Development

Contact: Prof. Dr. Martin Eilers, T (0931) 31-84442, martin.eilers@biozentrum.uni-wuerzburg.de

Gunnar Bartsch | idw
Further information:
http://www.uni-wuerzburg.de

Further reports about: Cancer Miz1 Myc Myc-Miz gene mutation genes human cell living organism mutated gene tumor growth

More articles from Life Sciences:

nachricht Warming ponds could accelerate climate change
21.02.2017 | University of Exeter

nachricht An alternative to opioids? Compound from marine snail is potent pain reliever
21.02.2017 | University of Utah

All articles from Life Sciences >>>

The most recent press releases about innovation >>>

Die letzten 5 Focus-News des innovations-reports im Überblick:

Im Focus: Breakthrough with a chain of gold atoms

In the field of nanoscience, an international team of physicists with participants from Konstanz has achieved a breakthrough in understanding heat transport

In the field of nanoscience, an international team of physicists with participants from Konstanz has achieved a breakthrough in understanding heat transport

Im Focus: DNA repair: a new letter in the cell alphabet

Results reveal how discoveries may be hidden in scientific “blind spots”

Cells need to repair damaged DNA in our genes to prevent the development of cancer and other diseases. Our cells therefore activate and send “repair-proteins”...

Im Focus: Dresdner scientists print tomorrow’s world

The Fraunhofer IWS Dresden and Technische Universität Dresden inaugurated their jointly operated Center for Additive Manufacturing Dresden (AMCD) with a festive ceremony on February 7, 2017. Scientists from various disciplines perform research on materials, additive manufacturing processes and innovative technologies, which build up components in a layer by layer process. This technology opens up new horizons for component design and combinations of functions. For example during fabrication, electrical conductors and sensors are already able to be additively manufactured into components. They provide information about stress conditions of a product during operation.

The 3D-printing technology, or additive manufacturing as it is often called, has long made the step out of scientific research laboratories into industrial...

Im Focus: Mimicking nature's cellular architectures via 3-D printing

Research offers new level of control over the structure of 3-D printed materials

Nature does amazing things with limited design materials. Grass, for example, can support its own weight, resist strong wind loads, and recover after being...

Im Focus: Three Magnetic States for Each Hole

Nanometer-scale magnetic perforated grids could create new possibilities for computing. Together with international colleagues, scientists from the Helmholtz Zentrum Dresden-Rossendorf (HZDR) have shown how a cobalt grid can be reliably programmed at room temperature. In addition they discovered that for every hole ("antidot") three magnetic states can be configured. The results have been published in the journal "Scientific Reports".

Physicist Dr. Rantej Bali from the HZDR, together with scientists from Singapore and Australia, designed a special grid structure in a thin layer of cobalt in...

All Focus news of the innovation-report >>>

Anzeige

Anzeige

Event News

Booth and panel discussion – The Lindau Nobel Laureate Meetings at the AAAS 2017 Annual Meeting

13.02.2017 | Event News

Complex Loading versus Hidden Reserves

10.02.2017 | Event News

International Conference on Crystal Growth in Freiburg

09.02.2017 | Event News

 
Latest News

Impacts of mass coral die-off on Indian Ocean reefs revealed

21.02.2017 | Earth Sciences

Novel breast tomosynthesis technique reduces screening recall rate

21.02.2017 | Medical Engineering

Use your Voice – and Smart Homes will “LISTEN”

21.02.2017 | Trade Fair News

VideoLinks
B2B-VideoLinks
More VideoLinks >>>